{"id":241,"date":"2014-11-12T22:02:18","date_gmt":"2014-11-12T22:02:18","guid":{"rendered":"http:\/\/courses.candelalearning.com\/novabiology\/?post_type=chapter&#038;p=241"},"modified":"2016-11-28T18:51:14","modified_gmt":"2016-11-28T18:51:14","slug":"characteristics-and-traits","status":"publish","type":"chapter","link":"https:\/\/courses.lumenlearning.com\/suny-biology1\/chapter\/characteristics-and-traits\/","title":{"raw":"Characteristics and Traits","rendered":"Characteristics and Traits"},"content":{"raw":"<div class=\"textbox learning-objectives\">\r\n<h3>Learning Objectives<\/h3>\r\nBy the end of this section, you will be able to:\r\n<ul>\r\n \t<li>Explain the relationship between genotypes and phenotypes in dominant and recessive gene systems<\/li>\r\n \t<li>Develop a Punnett square to calculate the expected proportions of genotypes and phenotypes in a monohybrid cross<\/li>\r\n \t<li>Explain the purpose and methods of a test cross<\/li>\r\n \t<li>Identify non-Mendelian inheritance patterns such as incomplete dominance, codominance, recessive lethals, multiple alleles, and sex linkage<\/li>\r\n<\/ul>\r\n<\/div>\r\nThe seven characteristics that Mendel evaluated in his pea plants were each expressed as one of two versions, or traits. The physical expression of characteristics is accomplished through the expression of genes carried on chromosomes. The genetic makeup of peas consists of two similar or homologous copies of each chromosome, one from each parent. Each pair of homologous chromosomes has the same linear order of genes. In other words, peas are diploid organisms in that they have two copies of each chromosome. The same is true for many other plants and for virtually all animals. Diploid organisms utilize meiosis to produce haploid gametes, which contain one copy of each homologous chromosome that unite at fertilization to create a diploid zygote.\r\n\r\nFor cases in which a single gene controls a single characteristic, a diploid organism has two genetic copies that may or may not encode the same version of that characteristic. Gene variants that arise by mutation and exist at the same relative locations on homologous chromosomes are called <b>alleles<\/b>. Mendel examined the inheritance of genes with just two allele forms, but it is common to encounter more than two alleles for any given gene in a natural population.\r\n<h2>Phenotypes and Genotypes<\/h2>\r\nTwo alleles for a given gene in a diploid organism are expressed and interact to produce physical characteristics. The observable traits expressed by an organism are referred to as its <b>phenotype<\/b>. An organism\u2019s underlying genetic makeup, consisting of both physically visible and non-expressed alleles, is called its <b>genotype<\/b>. Mendel\u2019s hybridization experiments demonstrate the difference between phenotype and genotype. When true-breeding plants in which one parent had yellow pods and one had green pods were cross-fertilized, all of the F<sub>1<\/sub> hybrid offspring had yellow pods. That is, the hybrid offspring were phenotypically identical to the true-breeding parent with yellow pods. However, we know that the allele donated by the parent with green pods was not simply lost because it reappeared in some of the F<sub>2<\/sub> offspring. Therefore, the F<sub>1<\/sub> plants must have been genotypically different from the parent with yellow pods.\r\n\r\nThe P<sub>1<\/sub> plants that Mendel used in his experiments were each homozygous for the trait he was studying. Diploid organisms that are <b>homozygous<\/b> at a given gene, or locus, have two identical alleles for that gene on their homologous chromosomes. Mendel\u2019s parental pea plants always bred true because both of the gametes produced carried the same trait. When P<sub>1<\/sub> plants with contrasting traits were cross-fertilized, all of the offspring were <b>heterozygous<\/b> for the contrasting trait, meaning that their genotype reflected that they had different alleles for the gene being examined.\r\n<h3>Dominant and Recessive Alleles<\/h3>\r\nOur discussion of homozygous and heterozygous organisms brings us to why the F<sub>1<\/sub> heterozygous offspring were identical to one of the parents, rather than expressing both alleles. In all seven pea-plant characteristics, one of the two contrasting alleles was dominant, and the other was recessive. Mendel called the dominant allele the expressed unit factor; the recessive allele was referred to as the latent unit factor. We now know that these so-called unit factors are actually genes on homologous chromosome pairs. For a gene that is expressed in a dominant and recessive pattern, homozygous dominant and heterozygous organisms will look identical (that is, they will have different genotypes but the same phenotype). The recessive allele will only be observed in homozygous recessive individuals (Table 1).\r\n<table>\r\n<thead>\r\n<tr>\r\n<th colspan=\"2\">Table 1. Human Inheritance in Dominant and Recessive Patterns<\/th>\r\n<\/tr>\r\n<tr>\r\n<th>Dominant Traits<\/th>\r\n<th>Recessive Traits<\/th>\r\n<\/tr>\r\n<\/thead>\r\n<tbody>\r\n<tr>\r\n<td>Achondroplasia<\/td>\r\n<td>Albinism<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>Brachydactyly<\/td>\r\n<td>Cystic fibrosis<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>Huntington\u2019s disease<\/td>\r\n<td>Duchenne muscular dystrophy<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>Marfan syndrome<\/td>\r\n<td>Galactosemia<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>Neurofibromatosis<\/td>\r\n<td>Phenylketonuria<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>Widow\u2019s peak<\/td>\r\n<td>Sickle-cell anemia<\/td>\r\n<\/tr>\r\n<tr>\r\n<td>Wooly hair<\/td>\r\n<td>Tay-Sachs disease<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\nSeveral conventions exist for referring to genes and alleles. For the purposes of this chapter, we will abbreviate genes using the first letter of the gene\u2019s corresponding dominant trait. For example, violet is the dominant trait for a pea plant\u2019s flower color, so the flower-color gene would be abbreviated as <em>V<\/em> (note that it is customary to italicize gene designations). Furthermore, we will use uppercase and lowercase letters to represent dominant and recessive alleles, respectively. Therefore, we would refer to the genotype of a homozygous dominant pea plant with violet flowers as <em>VV<\/em>, a homozygous recessive pea plant with white flowers as <em>vv<\/em>, and a heterozygous pea plant with violet flowers as <em>Vv<\/em>.\r\n<h2>The Punnett Square Approach for a Monohybrid Cross<\/h2>\r\nWhen fertilization occurs between two true-breeding parents that differ in only one characteristic, the process is called a <b>monohybrid<\/b> cross, and the resulting offspring are monohybrids. Mendel performed seven monohybrid crosses involving contrasting traits for each characteristic. On the basis of his results in F<sub>1<\/sub> and F<sub>2<\/sub> generations, Mendel postulated that each parent in the monohybrid cross contributed one of two paired unit factors to each offspring, and every possible combination of unit factors was equally likely.\r\n\r\nTo demonstrate a monohybrid cross, consider the case of true-breeding pea plants with yellow versus green pea seeds. The dominant seed color is yellow; therefore, the parental genotypes were <em>YY<\/em> for the plants with yellow seeds and <em>yy<\/em> for the plants with green seeds, respectively. A <b>Punnett square<\/b>, devised by the British geneticist Reginald Punnett, can be drawn that applies the rules of probability to predict the possible outcomes of a genetic cross or mating and their expected frequencies. To prepare a Punnett square, all possible combinations of the parental alleles are listed along the top (for one parent) and side (for the other parent) of a grid, representing their meiotic segregation into haploid gametes. Then the combinations of egg and sperm are made in the boxes in the table to show which alleles are combining. Each box then represents the diploid genotype of a zygote, or fertilized egg, that could result from this mating. Because each possibility is equally likely, genotypic ratios can be determined from a Punnett square. If the pattern of inheritance (dominant or recessive) is known, the phenotypic ratios can be inferred as well. For a monohybrid cross of two true-breeding parents, each parent contributes one type of allele. In this case, only one genotype is possible. All offspring are <em>Yy<\/em> and have yellow seeds (Figure\u00a01).\r\n\r\n[caption id=\"attachment_1445\" align=\"aligncenter\" width=\"544\"]<img class=\"size-full wp-image-1445\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184030\/Figure_12_02_01.jpg\" alt=\"This illustration shows a monohybrid cross. In the P generation, one parent has a dominant yellow phenotype and the genotype YY, and the other parent has the recessive green phenotype and the genotype yy. Each parent produces one kind of gamete, resulting in an F_{1} generation with a dominant yellow phenotype and the genotype Yy. Self-pollination of the F_{1} generation results in an F_{2} generation with a 3 to 1 ratio of yellow to green peas. One out of three of the yellow pea plants has a dominant genotype of YY, and 2 out of 3 have the heterozygous phenotype Yy. The homozygous recessive plant has the green phenotype and the genotype yy.\" width=\"544\" height=\"784\" \/> Figure\u00a01. In the P generation, pea plants that are true-breeding for the dominant yellow phenotype are crossed with plants with the recessive green phenotype. This cross produces F<sub>1<\/sub> heterozygotes with a yellow phenotype. Punnett square analysis can be used to predict the genotypes of the F<sub>2<\/sub> generation.[\/caption]\r\n\r\nA self-cross of one of the <em>Yy<\/em> heterozygous offspring can be represented in a 2 \u00d7 2 Punnett square because each parent can donate one of two different alleles. Therefore, the offspring can potentially have one of four allele combinations: <em>YY<\/em>, <em>Yy<\/em>, <em>yY<\/em>, or <em>yy<\/em> (Figure\u00a01). Notice that there are two ways to obtain the <em>Yy<\/em> genotype: a <em>Y<\/em> from the egg and a <em>y<\/em> from the sperm, or a <em>y<\/em> from the egg and a <em>Y<\/em> from the sperm. Both of these possibilities must be counted. Recall that Mendel\u2019s pea-plant characteristics behaved in the same way in reciprocal crosses. Therefore, the two possible heterozygous combinations produce offspring that are genotypically and phenotypically identical despite their dominant and recessive alleles deriving from different parents. They are grouped together. Because fertilization is a random event, we expect each combination to be equally likely and for the offspring to exhibit a ratio of <em>YY<\/em>:<em>Yy<\/em>:<em>yy<\/em> genotypes of 1:2:1 (Figure\u00a01). Furthermore, because the <em>YY<\/em> and <em>Yy<\/em> offspring have yellow seeds and are phenotypically identical, applying the sum rule of probability, we expect the offspring to exhibit a phenotypic ratio of 3 yellow:1 green. Indeed, working with large sample sizes, Mendel observed approximately this ratio in every F<sub>2<\/sub> generation resulting from crosses for individual traits.\r\n\r\nMendel validated these results by performing an F<sub>3<\/sub> cross in which he self-crossed the dominant- and recessive-expressing F<sub>2<\/sub> plants. When he self-crossed the plants expressing green seeds, all of the offspring had green seeds, confirming that all green seeds had homozygous genotypes of <em>yy<\/em>. When he self-crossed the F<sub>2<\/sub> plants expressing yellow seeds, he found that one-third of the plants bred true, and two-thirds of the plants segregated at a 3:1 ratio of yellow:green seeds. In this case, the true-breeding plants had homozygous (<em>YY<\/em>) genotypes, whereas the segregating plants corresponded to the heterozygous (<em>Yy<\/em>) genotype. When these plants self-fertilized, the outcome was just like the F<sub>1<\/sub> self-fertilizing cross.\r\n<h3>The Test Cross Distinguishes the Dominant Phenotype<\/h3>\r\nBeyond predicting the offspring of a cross between known homozygous or heterozygous parents, Mendel also developed a way to determine whether an organism that expressed a dominant trait was a heterozygote or a homozygote. Called the <b>test cross<\/b>, this technique is still used by plant and animal breeders. In a test cross, the dominant-expressing organism is crossed with an organism that is homozygous recessive for the same characteristic. If the dominant-expressing organism is a homozygote, then all F<sub>1<\/sub> offspring will be heterozygotes expressing the dominant trait (Figure\u00a02). Alternatively, if the dominant expressing organism is a heterozygote, the F<sub>1<\/sub> offspring will exhibit a 1:1 ratio of heterozygotes and recessive homozygotes (Figure\u00a02). The test cross further validates Mendel\u2019s postulate that pairs of unit factors segregate equally.\r\n<div class=\"textbox key-takeaways\">\r\n<h3>Art Connection<\/h3>\r\n[caption id=\"attachment_1447\" align=\"aligncenter\" width=\"544\"]<img class=\"size-full wp-image-1447\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184115\/Figure_12_02_02.jpg\" alt=\"In a test cross, a parent with a dominant phenotype but unknown genotype is crossed with a recessive parent. If the parent with the unknown phenotype is homozygous dominant, all of the resulting offspring will have at least one dominant allele. If the parent with the unknown phenotype is heterozygous, fifty percent of the offspring will inherit a recessive allele from both parents and will have the recessive phenotype.\" width=\"544\" height=\"675\" \/> Figure\u00a02.\u00a0 A test cross can be performed to determine whether an organism expressing a dominant trait is a homozygote or a heterozygote.[\/caption]\r\n\r\nIn pea plants, round peas (<em>R<\/em>) are dominant to wrinkled peas (<em>r<\/em>). You do a test cross between a pea plant with wrinkled peas (genotype <em>rr<\/em>) and a plant of unknown genotype that has round peas. You end up with three plants, all which have round peas. From this data, can you tell if the round pea parent plant is homozygous dominant or heterozygous? If the round pea parent plant is heterozygous, what is the probability that a random sample of 3 progeny peas will all be round?\r\n\r\n<\/div>\r\nMany human diseases are genetically inherited. A healthy person in a family in which some members suffer from a recessive genetic disorder may want to know if he or she has the disease-causing gene and what risk exists of passing the disorder on to his or her offspring. Of course, doing a test cross in humans is unethical and impractical. Instead, geneticists use <b>pedigree analysis<\/b> to study the inheritance pattern of human genetic diseases (Figure\u00a03).\r\n<div class=\"textbox key-takeaways\">\r\n<h3>Art Connection<\/h3>\r\n[caption id=\"attachment_1448\" align=\"aligncenter\" width=\"544\"]<img class=\"size-full wp-image-1448\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184146\/Figure_12_02_03.jpg\" alt=\"This is a pedigree of a family that carries the recessive disorder alkaptonuria. In the second generation, an unaffected mother and an affected father have three children. One child has the disorder, so the genotype of the mother must be Aa and the genotype of the father is aa. One unaffected child goes on to have two children, one affected and one unaffected. Because her husband was not affected, she and her husband must both be heterozygous. The genotype of their unaffected child is unknown, and is designated A?. In the third generation, the other unaffected child had no offspring, and his genotype is therefore also unknown. The affected third-generation child goes on to have one child with the disorder. Her husband is unaffected and is labeled \u201c3.\u201d The first generation father is affected and is labeled \u201c1.\u201d The first generation mother is unaffected and is labeled \u201c2.\u201d The Art Connection question asks the genotype of the three numbered individuals. \" width=\"544\" height=\"478\" \/> Figure\u00a03. In this pedigree analysis for alkaptonuria, individuals with the disorder are indicated in blue and have the genotype aa. Unaffected individuals are indicated in yellow and have the genotype AA or Aa.[\/caption]\r\n\r\nAlkaptonuria is a recessive genetic disorder in which two amino acids, phenylalanine and tyrosine, are not properly metabolized. Affected individuals may have darkened skin and brown urine, and may suffer joint damage and other complications. Looking at Figure\u00a03, we can see that it is often possible to determine a person\u2019s genotype from the genotype of their offspring. For example, if neither parent has the disorder but their child does, they must be heterozygous. Two individuals on the pedigree have an unaffected phenotype but unknown genotype. Because they do not have the disorder, they must have at least one normal allele, so their genotype gets the \u201c<em>A?<\/em>\u201d designation.\r\n\r\nWhat are the genotypes of the individuals labeled 1, 2 and 3?\r\n\r\n<\/div>\r\n<h2>Alternatives to Dominance and Recessiveness<\/h2>\r\nMendel\u2019s experiments with pea plants suggested that: (1) two \u201cunits\u201d or alleles exist for every gene; (2) alleles maintain their integrity in each generation (no blending); and (3) in the presence of the dominant allele, the recessive allele is hidden and makes no contribution to the phenotype. Therefore, recessive alleles can be \u201ccarried\u201d and not expressed by individuals. Such heterozygous individuals are sometimes referred to as \u201ccarriers.\u201d Further genetic studies in other plants and animals have shown that much more complexity exists, but that the fundamental principles of Mendelian genetics still hold true. In the sections to follow, we consider some of the extensions of Mendelism. If Mendel had chosen an experimental system that exhibited these genetic complexities, it\u2019s possible that he would not have understood what his results meant.\r\n<h3>Incomplete Dominance<\/h3>\r\n[caption id=\"attachment_1449\" align=\"alignright\" width=\"350\"]<img class=\" wp-image-1449\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184218\/Figure_12_02_04.jpg\" alt=\"Photo is of a snapdragon with a pink flower.\" width=\"350\" height=\"466\" \/> Figure\u00a04. These pink flowers of a heterozygote snapdragon result from incomplete dominance. (credit: \u201cstorebukkebruse\u201d\/Flickr)[\/caption]\r\n\r\nMendel\u2019s results, that traits are inherited as dominant and recessive pairs, contradicted the view at that time that offspring exhibited a blend of their parents\u2019 traits. However, the heterozygote phenotype occasionally does appear to be intermediate between the two parents. For example, in the snapdragon, <em>Antirrhinum majus<\/em> (Figure), a cross between a homozygous parent with white flowers (<em>C<sup class=\"sup\">W<\/sup>C<sup class=\"sup\">W<\/sup><\/em>) and a homozygous parent with red flowers (<em>C<sup class=\"sup\">R<\/sup>C<sup class=\"sup\">R<\/sup><\/em>) will produce offspring with pink flowers (<em>C<sup class=\"sup\">R<\/sup>C<sup class=\"sup\">W<\/sup><\/em>). (Note that different genotypic abbreviations are used for Mendelian extensions to distinguish these patterns from simple dominance and recessiveness.) This pattern of inheritance is described as <b>incomplete dominance<\/b>, denoting the expression of two contrasting alleles such that the individual displays an intermediate phenotype. The allele for red flowers is incompletely dominant over the allele for white flowers. However, the results of a heterozygote self-cross can still be predicted, just as with Mendelian dominant and recessive crosses. In this case, the genotypic ratio would be 1 <em>C<sup class=\"sup\">R<\/sup>C<sup class=\"sup\">R<\/sup><\/em>:2 <em>C<sup class=\"sup\">R<\/sup>C<sup class=\"sup\">W<\/sup><\/em>:1 <em>C<sup class=\"sup\">W<\/sup>C<sup class=\"sup\">W<\/sup><\/em>, and the phenotypic ratio would be 1:2:1 for red:pink:white.\r\n<h3>Codominance<\/h3>\r\nA variation on incomplete dominance is <b>codominance<\/b>, in which both alleles for the same characteristic are simultaneously expressed in the heterozygote. An example of codominance is the MN blood groups of humans. The M and N alleles are expressed in the form of an M or N antigen present on the surface of red blood cells. Homozygotes (<em>L<sup class=\"sup\">M<\/sup>L<sup class=\"sup\">M<\/sup><\/em> and <em>L<sup class=\"sup\">N<\/sup>L<sup class=\"sup\">N<\/sup><\/em>) express either the M or the N allele, and heterozygotes (<em>L<sup class=\"sup\">M<\/sup>L<sup class=\"sup\">N<\/sup><\/em>) express both alleles equally. In a self-cross between heterozygotes expressing a codominant trait, the three possible offspring genotypes are phenotypically distinct. However, the 1:2:1 genotypic ratio characteristic of a Mendelian monohybrid cross still applies.\r\n<h3>Multiple Alleles<\/h3>\r\nMendel implied that only two alleles, one dominant and one recessive, could exist for a given gene. We now know that this is an oversimplification. Although individual humans (and all diploid organisms) can only have two alleles for a given gene, multiple alleles may exist at the population level such that many combinations of two alleles are observed. Note that when many alleles exist for the same gene, the convention is to denote the most common phenotype or genotype among wild animals as the <b>wild type<\/b> (often abbreviated \u201c+\u201d); this is considered the standard or norm. All other phenotypes or genotypes are considered <b>variants<\/b> of this standard, meaning that they deviate from the wild type. The variant may be recessive or dominant to the wild-type allele.\r\n\r\nAn example of multiple alleles is coat color in rabbits (Figure\u00a05). Here, four alleles exist for the <em>c<\/em> gene. The wild-type version, <em>C<sup class=\"sup\">+<\/sup>C<sup class=\"sup\">+<\/sup><\/em>, is expressed as brown fur. The chinchilla phenotype, <em>c<sup class=\"sup\">ch<\/sup>c<sup class=\"sup\">ch<\/sup><\/em>, is expressed as black-tipped white fur. The Himalayan phenotype, <em>c<sup class=\"sup\">h<\/sup>c<sup class=\"sup\">h<\/sup><\/em>, has black fur on the extremities and white fur elsewhere. Finally, the albino, or \u201ccolorless\u201d phenotype, <em>cc<\/em>, is expressed as white fur. In cases of multiple alleles, dominance hierarchies can exist. In this case, the wild-type allele is dominant over all the others, chinchilla is incompletely dominant over Himalayan and albino, and Himalayan is dominant over albino. This hierarchy, or allelic series, was revealed by observing the phenotypes of each possible heterozygote offspring.\r\n\r\n[caption id=\"attachment_1450\" align=\"aligncenter\" width=\"800\"]<img class=\"size-full wp-image-1450\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184300\/Figure_12_02_05.jpg\" alt=\"This illustration shows the four different variants for coat color in rabbits at the c allele. The genotype CC produces the wild type phenotype, which is brown. The genotype c^{ch}c^{ch} produces the chinchilla phenotype, which is black-tipped white fur. The genotype c^{h}c^{h} produces the Himalayan phenotype, which is white on the body and black on the extremities. The genotype cc produces the recessive phenotype, which is white\" width=\"800\" height=\"574\" \/> Figure\u00a05. Four different alleles exist for the rabbit coat color (C) gene.[\/caption]\r\n\r\n[caption id=\"attachment_1451\" align=\"alignright\" width=\"350\"]<img class=\" wp-image-1451\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184330\/Figure_12_02_06.jpg\" alt=\"This photo shows Drosophila that has normal antennae on its head, and a mutant that has legs on its head.\" width=\"350\" height=\"345\" \/> Figure\u00a06. As seen in comparing the wild-type Drosophila (left) and the Antennapedia mutant (right), the Antennapedia mutant has legs on its head in place of antennae.[\/caption]\r\n\r\nThe complete dominance of a wild-type phenotype over all other mutants often occurs as an effect of \u201cdosage\u201d of a specific gene product, such that the wild-type allele supplies the correct amount of gene product whereas the mutant alleles cannot. For the allelic series in rabbits, the wild-type allele may supply a given dosage of fur pigment, whereas the mutants supply a lesser dosage or none at all. Interestingly, the Himalayan phenotype is the result of an allele that produces a temperature-sensitive gene product that only produces pigment in the cooler extremities of the rabbit\u2019s body.\r\n\r\nAlternatively, one mutant allele can be dominant over all other phenotypes, including the wild type. This may occur when the mutant allele somehow interferes with the genetic message so that even a heterozygote with one wild-type allele copy expresses the mutant phenotype. One way in which the mutant allele can interfere is by enhancing the function of the wild-type gene product or changing its distribution in the body. One example of this is the <em>Antennapedia<\/em> mutation in <em>Drosophila<\/em> (Figure\u00a06). In this case, the mutant allele expands the distribution of the gene product, and as a result, the <em>Antennapedia<\/em> heterozygote develops legs on its head where its antennae should be.\r\n<div class=\"textbox key-takeaways\">\r\n<h3>Evolution Connection<\/h3>\r\n<h4>Multiple Alleles Confer Drug Resistance in the Malaria Parasite<\/h4>\r\nMalaria is a parasitic disease in humans that is transmitted by infected female mosquitoes, including <em>Anopheles gambiae<\/em> (Figure<strong class=\"emphasis\" data-effect=\"bold\">\u00a0<\/strong>7a), and is characterized by cyclic high fevers, chills, flu-like symptoms, and severe anemia. <em>Plasmodium falciparum<\/em> and <em>P. vivax<\/em> are the most common causative agents of malaria, and <em>P. falciparum<\/em> is the most deadly (Figure\u00a07b)<em>.<\/em> When promptly and correctly treated, <em>P. falciparum<\/em> malaria has a mortality rate of 0.1 percent. However, in some parts of the world, the parasite has evolved resistance to commonly used malaria treatments, so the most effective malarial treatments can vary by geographic region.\r\n\r\n[caption id=\"attachment_1452\" align=\"aligncenter\" width=\"707\"]<img class=\"size-full wp-image-1452\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184426\/Figure_12_02_07.png\" alt=\"Photo a shows the Anopheles gambiae mosquito, which carries malaria. Photo b shows a micrograph of sickle-shaped Plasmodium falciparum, the parasite that causes malaria. The Plasmodium is about 0.75 microns across.\" width=\"707\" height=\"326\" \/> Figure\u00a07. The (a) Anopheles gambiae, or African malaria mosquito, acts as a vector in the transmission to humans of the malaria-causing parasite (b) Plasmodium falciparum, here visualized using false-color transmission electron microscopy. (credit a: James D. Gathany; credit b: Ute Frevert; false color by Margaret Shear; scale-bar data from Matt Russell)[\/caption]\r\n\r\nIn Southeast Asia, Africa, and South America, <em>P. falciparum<\/em> has developed resistance to the anti-malarial drugs chloroquine, mefloquine, and sulfadoxine-pyrimethamine. <em>P. falciparum<\/em>, which is haploid during the life stage in which it is infectious to humans, has evolved multiple drug-resistant mutant alleles of the <em>dhps<\/em> gene. Varying degrees of sulfadoxine resistance are associated with each of these alleles. Being haploid, <em>P. falciparum<\/em> needs only one drug-resistant allele to express this trait.\r\n\r\nIn Southeast Asia, different sulfadoxine-resistant alleles of the <em>dhps<\/em> gene are localized to different geographic regions. This is a common evolutionary phenomenon that occurs because drug-resistant mutants arise in a population and interbreed with other <em>P. falciparum<\/em> isolates in close proximity. Sulfadoxine-resistant parasites cause considerable human hardship in regions where this drug is widely used as an over-the-counter malaria remedy. As is common with pathogens that multiply to large numbers within an infection cycle, <em>P. falciparum<\/em> evolves relatively rapidly (over a decade or so) in response to the selective pressure of commonly used anti-malarial drugs. For this reason, scientists must constantly work to develop new drugs or drug combinations to combat the worldwide malaria burden.[footnote]Sumiti Vinayak, et al., \u201cOrigin and Evolution of Sulfadoxine Resistant Plasmodium falciparum,\u201d Public Library of Science Pathogens 6, no. 3 (2010): e1000830, doi:10.1371\/journal.ppat.1000830.[\/footnote]\r\n\r\n<\/div>\r\n<h2>X-Linked Traits<\/h2>\r\nIn humans, as well as in many other animals and some plants, the sex of the individual is determined by sex chromosomes. The sex chromosomes are one pair of non-homologous chromosomes. Until now, we have only considered inheritance patterns among non-sex chromosomes, or <b>autosomes<\/b>. In addition to 22 homologous pairs of autosomes, human females have a homologous pair of X chromosomes, whereas human males have an XY chromosome pair. Although the Y chromosome contains a small region of similarity to the X chromosome so that they can pair during meiosis, the Y chromosome is much shorter and contains many fewer genes. When a gene being examined is present on the X chromosome, but not on the Y chromosome, it is said to be <b>X-linked<\/b>.\r\n\r\n[caption id=\"attachment_1453\" align=\"alignright\" width=\"350\"]<img class=\"wp-image-1453\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184500\/Figure_12_02_08.jpeg\" alt=\"Photo shows six fruit flies, each with a different eye color.\" width=\"350\" height=\"439\" \/> Figure\u00a08. In Drosophila, the gene for eye color is located on the X chromosome. Clockwise from top left are brown, cinnabar, sepia, vermilion, white, and red. Red eye color is wild-type and is dominant to white eye color.[\/caption]\r\n\r\nEye color in <em>Drosophila<\/em> was one of the first X-linked traits to be identified. Thomas Hunt Morgan mapped this trait to the X chromosome in 1910. Like humans, <em>Drosophila<\/em> males have an XY chromosome pair, and females are XX. In flies, the wild-type eye color is red (X<sup class=\"sup\"><em>W<\/em><\/sup>) and it is dominant to white eye color (X<sup class=\"sup\"><em>w<\/em><\/sup>) (Figure\u00a08). Because of the location of the eye-color gene, reciprocal crosses do not produce the same offspring ratios. Males are said to be <b>hemizygous<\/b>, because they have only one allele for any X-linked characteristic. Hemizygosity makes the descriptions of dominance and recessiveness irrelevant for XY males. <em>Drosophila<\/em> males lack a second allele copy on the Y chromosome; that is, their genotype can only be X<sup class=\"sup\"><em>W<\/em><\/sup>Y or X<sup class=\"sup\"><em>w<\/em><\/sup>Y. In contrast, females have two allele copies of this gene and can be X<sup class=\"sup\"><em>W<\/em><\/sup>X<sup class=\"sup\"><em>W<\/em><\/sup>, X<sup class=\"sup\"><em>W<\/em><\/sup>X<sup class=\"sup\"><em>w<\/em><\/sup>, or X<sup class=\"sup\"><em>w<\/em><\/sup>X<sup class=\"sup\"><em>w<\/em><\/sup>.\r\n\r\nIn an X-linked cross, the genotypes of F<sub>1<\/sub> and F<sub>2<\/sub> offspring depend on whether the recessive trait was expressed by the male or the female in the P<sub>1<\/sub> generation. With regard to <em>Drosophila<\/em> eye color, when the P<sub>1<\/sub> male expresses the white-eye phenotype and the female is homozygous red-eyed, all members of the F<sub>1<\/sub> generation exhibit red eyes (Figure). The F<sub>1<\/sub> females are heterozygous (X<em><sup class=\"sup\">W<\/sup><\/em>X<em><sup class=\"sup\">w<\/sup><\/em>), and the males are all X<em><sup class=\"sup\">W<\/sup><\/em>Y, having received their X chromosome from the homozygous dominant P<sub>1<\/sub> female and their Y chromosome from the P<sub>1<\/sub> male. A subsequent cross between the X<em><sup class=\"sup\">W<\/sup><\/em>X<em><sup class=\"sup\">w<\/sup><\/em> female and the X<em><sup class=\"sup\">W<\/sup><\/em>Y male would produce only red-eyed females (with X<em><sup class=\"sup\">W<\/sup><\/em>X<em><sup class=\"sup\">W<\/sup><\/em> or X<em><sup class=\"sup\">W<\/sup><\/em>X<em><sup class=\"sup\">w<\/sup><\/em> genotypes) and both red- and white-eyed males (with X<em><sup class=\"sup\">W<\/sup><\/em>Y or X<em><sup class=\"sup\">w<\/sup><\/em>Y genotypes). Now, consider a cross between a homozygous white-eyed female and a male with red eyes. The F<sub>1<\/sub> generation would exhibit only heterozygous red-eyed females (X<em><sup class=\"sup\">W<\/sup><\/em>X<em><sup class=\"sup\">w<\/sup><\/em>) and only white-eyed males (X<em><sup class=\"sup\">w<\/sup><\/em>Y). Half of the F<sub>2<\/sub> females would be red-eyed (X<em><sup class=\"sup\">W<\/sup><\/em>X<em><sup class=\"sup\">w<\/sup><\/em>) and half would be white-eyed (X<em><sup class=\"sup\">w<\/sup><\/em>X<em><sup class=\"sup\">w<\/sup><\/em>). Similarly, half of the F<sub>2<\/sub> males would be red-eyed (X<em><sup class=\"sup\">W<\/sup><\/em>Y) and half would be white-eyed (X<em><sup class=\"sup\">w<\/sup><\/em>Y).\r\n<div class=\"textbox key-takeaways\">\r\n<h3>Art Connection<\/h3>\r\n[caption id=\"attachment_1454\" align=\"aligncenter\" width=\"725\"]<img class=\"size-full wp-image-1454\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184601\/Figure_12_02_09.jpeg\" alt=\"This illustration shows a Punnett square analysis of fruit fly eye color, which is a sex-linked trait. A red-eyed male fruit fly with the genotype X^{w}Y is crossed with a white-eyed female fruit fly with the genotype X^{w}X^{w}. All of the female offspring acquire a dominant W allele from the father and a recessive w allele from the mother, and are therefore heterozygous dominant with red eye color. All of the male offspring acquire a recessive w allele from the mother and a Y chromosome from the father and are therefore hemizygous recessive with white eye color.\" width=\"725\" height=\"729\" \/> Figure\u00a09. Punnett square analysis is used to determine the ratio of offspring from a cross between a red-eyed male fruit fly and a white-eyed female fruit fly.[\/caption]\r\n\r\nWhat ratio of offspring would result from a cross between a white-eyed male and a female that is heterozygous for red eye color?\r\n\r\n<\/div>\r\nDiscoveries in fruit fly genetics can be applied to human genetics. When a female parent is homozygous for a recessive X-linked trait, she will pass the trait on to 100 percent of her offspring. Her male offspring are, therefore, destined to express the trait, as they will inherit their father's Y chromosome. In humans, the alleles for certain conditions (some forms of color blindness, hemophilia, and muscular dystrophy) are X-linked. Females who are heterozygous for these diseases are said to be carriers and may not exhibit any phenotypic effects. These females will pass the disease to half of their sons and will pass carrier status to half of their daughters; therefore, recessive X-linked traits appear more frequently in males than females.\r\n\r\nIn some groups of organisms with sex chromosomes, the gender with the non-homologous sex chromosomes is the female rather than the male. This is the case for all birds. In this case, sex-linked traits will be more likely to appear in the female, in which they are hemizygous.\r\n<h2>Human Sex-linked Disorders<\/h2>\r\nSex-linkage studies in Morgan\u2019s laboratory provided the fundamentals for understanding X-linked recessive disorders in humans, which include red-green color blindness, and Types A and B hemophilia. Because human males need to inherit only one recessive mutant X allele to be affected, X-linked disorders are disproportionately observed in males. Females must inherit recessive X-linked alleles from both of their parents in order to express the trait. When they inherit one recessive X-linked mutant allele and one dominant X-linked wild-type allele, they are carriers of the trait and are typically unaffected. Carrier females can manifest mild forms of the trait due to the inactivation of the dominant allele located on one of the X chromosomes. However, female carriers can contribute the trait to their sons, resulting in the son exhibiting the trait, or they can contribute the recessive allele to their daughters, resulting in the daughters being carriers of the trait (Figure\u00a010). Although some Y-linked recessive disorders exist, typically they are associated with infertility in males and are therefore not transmitted to subsequent generations.\r\n\r\n[caption id=\"attachment_1455\" align=\"aligncenter\" width=\"655\"]<img class=\"size-full wp-image-1455\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184635\/Figure_12_02_10.jpeg\" alt=\"A diagram shows an unaffected father with a dominant allele and an unaffected carrier mother with an x-linked recessive allele. Four figures of offspring are shown representing the various resulting genetic combinations: unaffected son, unaffected daughter, affected son, and unaffected carrier daughter.\" width=\"655\" height=\"719\" \/> Figure\u00a010. The son of a woman who is a carrier of a recessive X-linked disorder will have a 50 percent chance of being affected. A daughter will not be affected, but she will have a 50 percent chance of being a carrier like her mother.[\/caption]\r\n\r\n<div class=\"textbox shaded\">\r\n<h3>Link to Learning<\/h3>\r\nWatch this video to learn more about sex-linked traits.\r\n\r\nhttps:\/\/youtu.be\/-ROhfKyxgCo\r\n\r\n<\/div>\r\n<h2>Lethality<\/h2>\r\nA large proportion of genes in an individual\u2019s genome are essential for survival. Occasionally, a nonfunctional allele for an essential gene can arise by mutation and be transmitted in a population as long as individuals with this allele also have a wild-type, functional copy. The wild-type allele functions at a capacity sufficient to sustain life and is therefore considered to be dominant over the nonfunctional allele. However, consider two heterozygous parents that have a genotype of wild-type\/nonfunctional mutant for a hypothetical essential gene. In one quarter of their offspring, we would expect to observe individuals that are homozygous recessive for the nonfunctional allele. Because the gene is essential, these individuals might fail to develop past fertilization, die <em>in utero<\/em>, or die later in life, depending on what life stage requires this gene. An inheritance pattern in which an allele is only lethal in the homozygous form and in which the heterozygote may be normal or have some altered non-lethal phenotype is referred to as <b>recessive lethal<\/b>.\r\n\r\nFor crosses between heterozygous individuals with a recessive lethal allele that causes death before birth when homozygous, only wild-type homozygotes and heterozygotes would be observed. The genotypic ratio would therefore be 2:1. In other instances, the recessive lethal allele might also exhibit a dominant (but not lethal) phenotype in the heterozygote. For instance, the recessive lethal <em>Curly<\/em> allele in <em>Drosophila<\/em> affects wing shape in the heterozygote form but is lethal in the homozygote.\r\n\r\n[caption id=\"attachment_1456\" align=\"alignright\" width=\"300\"]<img class=\"wp-image-1456\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184712\/Figure_12_02_11.jpeg\" alt=\"Micrograph shows a neuron with nuclear inclusions characteristic of Huntington\u2019s disease.\" width=\"300\" height=\"389\" \/> Figure\u00a011. The neuron in the center of this micrograph (yellow) has nuclear inclusions characteristic of Huntington\u2019s disease (orange area in the center of the neuron). Huntington\u2019s disease occurs when an abnormal dominant allele for the Huntington gene is present. (credit: Dr. Steven Finkbeiner, Gladstone Institute of Neurological Disease, The Taube-Koret Center for Huntington's Disease Research, and the University of California San Francisco\/Wikimedia)[\/caption]\r\n\r\nA single copy of the wild-type allele is not always sufficient for normal functioning or even survival. The <b>dominant lethal<\/b> inheritance pattern is one in which an allele is lethal both in the homozygote and the heterozygote; this allele can only be transmitted if the lethality phenotype occurs after reproductive age. Individuals with mutations that result in dominant lethal alleles fail to survive even in the heterozygote form. Dominant lethal alleles are very rare because, as you might expect, the allele only lasts one generation and is not transmitted. However, just as the recessive lethal allele might not immediately manifest the phenotype of death, dominant lethal alleles also might not be expressed until adulthood. Once the individual reaches reproductive age, the allele may be unknowingly passed on, resulting in a delayed death in both generations. An example of this in humans is Huntington\u2019s disease, in which the nervous system gradually wastes away (Figure\u00a011). People who are heterozygous for the dominant Huntington allele (<em>Hh<\/em>) will inevitably develop the fatal disease. However, the onset of Huntington\u2019s disease may not occur until age 40, at which point the afflicted persons may have already passed the allele to 50 percent of their offspring.\r\n<h2>Section Summary<\/h2>\r\nWhen true-breeding or homozygous individuals that differ for a certain trait are crossed, all of the offspring will be heterozygotes for that trait. If the traits are inherited as dominant and recessive, the F<sub>1<\/sub> offspring will all exhibit the same phenotype as the parent homozygous for the dominant trait. If these heterozygous offspring are self-crossed, the resulting F<sub>2<\/sub> offspring will be equally likely to inherit gametes carrying the dominant or recessive trait, giving rise to offspring of which one quarter are homozygous dominant, half are heterozygous, and one quarter are homozygous recessive. Because homozygous dominant and heterozygous individuals are phenotypically identical, the observed traits in the F<sub>2<\/sub> offspring will exhibit a ratio of three dominant to one recessive.\r\n\r\nAlleles do not always behave in dominant and recessive patterns. Incomplete dominance describes situations in which the heterozygote exhibits a phenotype that is intermediate between the homozygous phenotypes. Codominance describes the simultaneous expression of both of the alleles in the heterozygote. Although diploid organisms can only have two alleles for any given gene, it is common for more than two alleles of a gene to exist in a population. In humans, as in many animals and some plants, females have two X chromosomes and males have one X and one Y chromosome. Genes that are present on the X but not the Y chromosome are said to be X-linked, such that males only inherit one allele for the gene, and females inherit two. Finally, some alleles can be lethal. Recessive lethal alleles are only lethal in homozygotes, but dominant lethal alleles are fatal in heterozygotes as well.\r\n<div class=\"textbox exercises\">\r\n<h3>Additional Self Check Questions<\/h3>\r\n<ol>\r\n \t<li>In pea plants, round peas (<em>R<\/em>) are dominant to wrinkled peas (<em>r<\/em>). You do a test cross between a pea plant with wrinkled peas (genotype <em>rr<\/em>) and a plant of unknown genotype that has round peas. You end up with three plants, all which have round peas. From this data, can you tell if the round pea parent plant is homozygous dominant or heterozygous? If the round pea parent plant is heterozygous, what is the probability that a random sample of 3 progeny peas will all be round?<\/li>\r\n \t<li>What are the genotypes of the individuals labeled 1, 2 and 3?<\/li>\r\n \t<li>What ratio of offspring would result from a cross between a white-eyed male and a female that is heterozygous for red eye color?<\/li>\r\n \t<li>The gene for flower position in pea plants exists as axial or terminal alleles. Given that axial is dominant to terminal, list all of the possible F<sub>1<\/sub> and F<sub>2<\/sub> genotypes and phenotypes from a cross involving parents that are homozygous for each trait. Express genotypes with conventional genetic abbreviations.<\/li>\r\n \t<li>Use a Punnett square to predict the offspring in a cross between a dwarf pea plant (homozygous recessive) and a tall pea plant (heterozygous). What is the phenotypic ratio of the offspring?<\/li>\r\n \t<li>Can a human male be a carrier of red-green color blindness?<\/li>\r\n<\/ol>\r\n<\/div>\r\n<div class=\"textbox exercises\">\r\n<h3>Answers<\/h3>\r\n<ol>\r\n \t<li>You cannot be sure if the plant is homozygous or heterozygous as the data set is too small: by random chance, all three plants might have acquired only the dominant gene even if the recessive one is present. If the round pea parent is heterozygous, there is a one-eighth probability that a random sample of three progeny peas will all be round.<\/li>\r\n \t<li>Individual 1 has the genotype <em>aa<\/em>. Individual 2 has the genotype <em>Aa<\/em>. Individual 3 has the genotype <em>Aa<\/em>.<\/li>\r\n \t<li>Half of the female offspring would be heterozygous (X<sup class=\"sup\"><em>W<\/em><\/sup>X<sup class=\"sup\"><em>w<\/em><\/sup>) with red eyes, and half would be homozygous recessive (X<sup class=\"sup\"><em>w<\/em><\/sup>X<sup class=\"sup\"><em>w<\/em><\/sup>) with white eyes. Half of the male offspring would be hemizygous dominant (X<sup class=\"sup\"><em>W<\/em><\/sup>Y) withe red yes, and half would be hemizygous recessive (X<sup class=\"sup\"><em>w<\/em><\/sup>Y) with white eyes.<\/li>\r\n \t<li>Because axial is dominant, the gene would be designated as <em>A<\/em>. F<sub>1<\/sub> would be all heterozygous <em>Aa<\/em> with axial phenotype. F<sub>2<\/sub> would have possible genotypes of <em>AA<\/em>, <em>Aa<\/em>, and <em>aa<\/em>; these would correspond to axial, axial, and terminal phenotypes, respectively.<\/li>\r\n \t<li>The Punnett square would be 2 \u00d7 2 and will have <em>T<\/em> and <em>T<\/em> along the top, and <em>T<\/em> and <em>t<\/em> along the left side. Clockwise from the top left, the genotypes listed within the boxes will be <em>Tt<\/em>, <em>Tt<\/em>, <em>tt<\/em>, and <em>tt<\/em>. The phenotypic ratio will be 1 tall:1 dwarf.<\/li>\r\n \t<li>No, males can only express color blindness. They cannot carry it because an individual needs two X chromosomes to be a carrier.<\/li>\r\n<\/ol>\r\n<\/div>","rendered":"<div class=\"textbox learning-objectives\">\n<h3>Learning Objectives<\/h3>\n<p>By the end of this section, you will be able to:<\/p>\n<ul>\n<li>Explain the relationship between genotypes and phenotypes in dominant and recessive gene systems<\/li>\n<li>Develop a Punnett square to calculate the expected proportions of genotypes and phenotypes in a monohybrid cross<\/li>\n<li>Explain the purpose and methods of a test cross<\/li>\n<li>Identify non-Mendelian inheritance patterns such as incomplete dominance, codominance, recessive lethals, multiple alleles, and sex linkage<\/li>\n<\/ul>\n<\/div>\n<p>The seven characteristics that Mendel evaluated in his pea plants were each expressed as one of two versions, or traits. The physical expression of characteristics is accomplished through the expression of genes carried on chromosomes. The genetic makeup of peas consists of two similar or homologous copies of each chromosome, one from each parent. Each pair of homologous chromosomes has the same linear order of genes. In other words, peas are diploid organisms in that they have two copies of each chromosome. The same is true for many other plants and for virtually all animals. Diploid organisms utilize meiosis to produce haploid gametes, which contain one copy of each homologous chromosome that unite at fertilization to create a diploid zygote.<\/p>\n<p>For cases in which a single gene controls a single characteristic, a diploid organism has two genetic copies that may or may not encode the same version of that characteristic. Gene variants that arise by mutation and exist at the same relative locations on homologous chromosomes are called <b>alleles<\/b>. Mendel examined the inheritance of genes with just two allele forms, but it is common to encounter more than two alleles for any given gene in a natural population.<\/p>\n<h2>Phenotypes and Genotypes<\/h2>\n<p>Two alleles for a given gene in a diploid organism are expressed and interact to produce physical characteristics. The observable traits expressed by an organism are referred to as its <b>phenotype<\/b>. An organism\u2019s underlying genetic makeup, consisting of both physically visible and non-expressed alleles, is called its <b>genotype<\/b>. Mendel\u2019s hybridization experiments demonstrate the difference between phenotype and genotype. When true-breeding plants in which one parent had yellow pods and one had green pods were cross-fertilized, all of the F<sub>1<\/sub> hybrid offspring had yellow pods. That is, the hybrid offspring were phenotypically identical to the true-breeding parent with yellow pods. However, we know that the allele donated by the parent with green pods was not simply lost because it reappeared in some of the F<sub>2<\/sub> offspring. Therefore, the F<sub>1<\/sub> plants must have been genotypically different from the parent with yellow pods.<\/p>\n<p>The P<sub>1<\/sub> plants that Mendel used in his experiments were each homozygous for the trait he was studying. Diploid organisms that are <b>homozygous<\/b> at a given gene, or locus, have two identical alleles for that gene on their homologous chromosomes. Mendel\u2019s parental pea plants always bred true because both of the gametes produced carried the same trait. When P<sub>1<\/sub> plants with contrasting traits were cross-fertilized, all of the offspring were <b>heterozygous<\/b> for the contrasting trait, meaning that their genotype reflected that they had different alleles for the gene being examined.<\/p>\n<h3>Dominant and Recessive Alleles<\/h3>\n<p>Our discussion of homozygous and heterozygous organisms brings us to why the F<sub>1<\/sub> heterozygous offspring were identical to one of the parents, rather than expressing both alleles. In all seven pea-plant characteristics, one of the two contrasting alleles was dominant, and the other was recessive. Mendel called the dominant allele the expressed unit factor; the recessive allele was referred to as the latent unit factor. We now know that these so-called unit factors are actually genes on homologous chromosome pairs. For a gene that is expressed in a dominant and recessive pattern, homozygous dominant and heterozygous organisms will look identical (that is, they will have different genotypes but the same phenotype). The recessive allele will only be observed in homozygous recessive individuals (Table 1).<\/p>\n<table>\n<thead>\n<tr>\n<th colspan=\"2\">Table 1. Human Inheritance in Dominant and Recessive Patterns<\/th>\n<\/tr>\n<tr>\n<th>Dominant Traits<\/th>\n<th>Recessive Traits<\/th>\n<\/tr>\n<\/thead>\n<tbody>\n<tr>\n<td>Achondroplasia<\/td>\n<td>Albinism<\/td>\n<\/tr>\n<tr>\n<td>Brachydactyly<\/td>\n<td>Cystic fibrosis<\/td>\n<\/tr>\n<tr>\n<td>Huntington\u2019s disease<\/td>\n<td>Duchenne muscular dystrophy<\/td>\n<\/tr>\n<tr>\n<td>Marfan syndrome<\/td>\n<td>Galactosemia<\/td>\n<\/tr>\n<tr>\n<td>Neurofibromatosis<\/td>\n<td>Phenylketonuria<\/td>\n<\/tr>\n<tr>\n<td>Widow\u2019s peak<\/td>\n<td>Sickle-cell anemia<\/td>\n<\/tr>\n<tr>\n<td>Wooly hair<\/td>\n<td>Tay-Sachs disease<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p>Several conventions exist for referring to genes and alleles. For the purposes of this chapter, we will abbreviate genes using the first letter of the gene\u2019s corresponding dominant trait. For example, violet is the dominant trait for a pea plant\u2019s flower color, so the flower-color gene would be abbreviated as <em>V<\/em> (note that it is customary to italicize gene designations). Furthermore, we will use uppercase and lowercase letters to represent dominant and recessive alleles, respectively. Therefore, we would refer to the genotype of a homozygous dominant pea plant with violet flowers as <em>VV<\/em>, a homozygous recessive pea plant with white flowers as <em>vv<\/em>, and a heterozygous pea plant with violet flowers as <em>Vv<\/em>.<\/p>\n<h2>The Punnett Square Approach for a Monohybrid Cross<\/h2>\n<p>When fertilization occurs between two true-breeding parents that differ in only one characteristic, the process is called a <b>monohybrid<\/b> cross, and the resulting offspring are monohybrids. Mendel performed seven monohybrid crosses involving contrasting traits for each characteristic. On the basis of his results in F<sub>1<\/sub> and F<sub>2<\/sub> generations, Mendel postulated that each parent in the monohybrid cross contributed one of two paired unit factors to each offspring, and every possible combination of unit factors was equally likely.<\/p>\n<p>To demonstrate a monohybrid cross, consider the case of true-breeding pea plants with yellow versus green pea seeds. The dominant seed color is yellow; therefore, the parental genotypes were <em>YY<\/em> for the plants with yellow seeds and <em>yy<\/em> for the plants with green seeds, respectively. A <b>Punnett square<\/b>, devised by the British geneticist Reginald Punnett, can be drawn that applies the rules of probability to predict the possible outcomes of a genetic cross or mating and their expected frequencies. To prepare a Punnett square, all possible combinations of the parental alleles are listed along the top (for one parent) and side (for the other parent) of a grid, representing their meiotic segregation into haploid gametes. Then the combinations of egg and sperm are made in the boxes in the table to show which alleles are combining. Each box then represents the diploid genotype of a zygote, or fertilized egg, that could result from this mating. Because each possibility is equally likely, genotypic ratios can be determined from a Punnett square. If the pattern of inheritance (dominant or recessive) is known, the phenotypic ratios can be inferred as well. For a monohybrid cross of two true-breeding parents, each parent contributes one type of allele. In this case, only one genotype is possible. All offspring are <em>Yy<\/em> and have yellow seeds (Figure\u00a01).<\/p>\n<div id=\"attachment_1445\" style=\"width: 554px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1445\" class=\"size-full wp-image-1445\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184030\/Figure_12_02_01.jpg\" alt=\"This illustration shows a monohybrid cross. In the P generation, one parent has a dominant yellow phenotype and the genotype YY, and the other parent has the recessive green phenotype and the genotype yy. Each parent produces one kind of gamete, resulting in an F_{1} generation with a dominant yellow phenotype and the genotype Yy. Self-pollination of the F_{1} generation results in an F_{2} generation with a 3 to 1 ratio of yellow to green peas. One out of three of the yellow pea plants has a dominant genotype of YY, and 2 out of 3 have the heterozygous phenotype Yy. The homozygous recessive plant has the green phenotype and the genotype yy.\" width=\"544\" height=\"784\" \/><\/p>\n<p id=\"caption-attachment-1445\" class=\"wp-caption-text\">Figure\u00a01. In the P generation, pea plants that are true-breeding for the dominant yellow phenotype are crossed with plants with the recessive green phenotype. This cross produces F<sub>1<\/sub> heterozygotes with a yellow phenotype. Punnett square analysis can be used to predict the genotypes of the F<sub>2<\/sub> generation.<\/p>\n<\/div>\n<p>A self-cross of one of the <em>Yy<\/em> heterozygous offspring can be represented in a 2 \u00d7 2 Punnett square because each parent can donate one of two different alleles. Therefore, the offspring can potentially have one of four allele combinations: <em>YY<\/em>, <em>Yy<\/em>, <em>yY<\/em>, or <em>yy<\/em> (Figure\u00a01). Notice that there are two ways to obtain the <em>Yy<\/em> genotype: a <em>Y<\/em> from the egg and a <em>y<\/em> from the sperm, or a <em>y<\/em> from the egg and a <em>Y<\/em> from the sperm. Both of these possibilities must be counted. Recall that Mendel\u2019s pea-plant characteristics behaved in the same way in reciprocal crosses. Therefore, the two possible heterozygous combinations produce offspring that are genotypically and phenotypically identical despite their dominant and recessive alleles deriving from different parents. They are grouped together. Because fertilization is a random event, we expect each combination to be equally likely and for the offspring to exhibit a ratio of <em>YY<\/em>:<em>Yy<\/em>:<em>yy<\/em> genotypes of 1:2:1 (Figure\u00a01). Furthermore, because the <em>YY<\/em> and <em>Yy<\/em> offspring have yellow seeds and are phenotypically identical, applying the sum rule of probability, we expect the offspring to exhibit a phenotypic ratio of 3 yellow:1 green. Indeed, working with large sample sizes, Mendel observed approximately this ratio in every F<sub>2<\/sub> generation resulting from crosses for individual traits.<\/p>\n<p>Mendel validated these results by performing an F<sub>3<\/sub> cross in which he self-crossed the dominant- and recessive-expressing F<sub>2<\/sub> plants. When he self-crossed the plants expressing green seeds, all of the offspring had green seeds, confirming that all green seeds had homozygous genotypes of <em>yy<\/em>. When he self-crossed the F<sub>2<\/sub> plants expressing yellow seeds, he found that one-third of the plants bred true, and two-thirds of the plants segregated at a 3:1 ratio of yellow:green seeds. In this case, the true-breeding plants had homozygous (<em>YY<\/em>) genotypes, whereas the segregating plants corresponded to the heterozygous (<em>Yy<\/em>) genotype. When these plants self-fertilized, the outcome was just like the F<sub>1<\/sub> self-fertilizing cross.<\/p>\n<h3>The Test Cross Distinguishes the Dominant Phenotype<\/h3>\n<p>Beyond predicting the offspring of a cross between known homozygous or heterozygous parents, Mendel also developed a way to determine whether an organism that expressed a dominant trait was a heterozygote or a homozygote. Called the <b>test cross<\/b>, this technique is still used by plant and animal breeders. In a test cross, the dominant-expressing organism is crossed with an organism that is homozygous recessive for the same characteristic. If the dominant-expressing organism is a homozygote, then all F<sub>1<\/sub> offspring will be heterozygotes expressing the dominant trait (Figure\u00a02). Alternatively, if the dominant expressing organism is a heterozygote, the F<sub>1<\/sub> offspring will exhibit a 1:1 ratio of heterozygotes and recessive homozygotes (Figure\u00a02). The test cross further validates Mendel\u2019s postulate that pairs of unit factors segregate equally.<\/p>\n<div class=\"textbox key-takeaways\">\n<h3>Art Connection<\/h3>\n<div id=\"attachment_1447\" style=\"width: 554px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1447\" class=\"size-full wp-image-1447\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184115\/Figure_12_02_02.jpg\" alt=\"In a test cross, a parent with a dominant phenotype but unknown genotype is crossed with a recessive parent. If the parent with the unknown phenotype is homozygous dominant, all of the resulting offspring will have at least one dominant allele. If the parent with the unknown phenotype is heterozygous, fifty percent of the offspring will inherit a recessive allele from both parents and will have the recessive phenotype.\" width=\"544\" height=\"675\" \/><\/p>\n<p id=\"caption-attachment-1447\" class=\"wp-caption-text\">Figure\u00a02.\u00a0 A test cross can be performed to determine whether an organism expressing a dominant trait is a homozygote or a heterozygote.<\/p>\n<\/div>\n<p>In pea plants, round peas (<em>R<\/em>) are dominant to wrinkled peas (<em>r<\/em>). You do a test cross between a pea plant with wrinkled peas (genotype <em>rr<\/em>) and a plant of unknown genotype that has round peas. You end up with three plants, all which have round peas. From this data, can you tell if the round pea parent plant is homozygous dominant or heterozygous? If the round pea parent plant is heterozygous, what is the probability that a random sample of 3 progeny peas will all be round?<\/p>\n<\/div>\n<p>Many human diseases are genetically inherited. A healthy person in a family in which some members suffer from a recessive genetic disorder may want to know if he or she has the disease-causing gene and what risk exists of passing the disorder on to his or her offspring. Of course, doing a test cross in humans is unethical and impractical. Instead, geneticists use <b>pedigree analysis<\/b> to study the inheritance pattern of human genetic diseases (Figure\u00a03).<\/p>\n<div class=\"textbox key-takeaways\">\n<h3>Art Connection<\/h3>\n<div id=\"attachment_1448\" style=\"width: 554px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1448\" class=\"size-full wp-image-1448\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184146\/Figure_12_02_03.jpg\" alt=\"This is a pedigree of a family that carries the recessive disorder alkaptonuria. In the second generation, an unaffected mother and an affected father have three children. One child has the disorder, so the genotype of the mother must be Aa and the genotype of the father is aa. One unaffected child goes on to have two children, one affected and one unaffected. Because her husband was not affected, she and her husband must both be heterozygous. The genotype of their unaffected child is unknown, and is designated A?. In the third generation, the other unaffected child had no offspring, and his genotype is therefore also unknown. The affected third-generation child goes on to have one child with the disorder. Her husband is unaffected and is labeled \u201c3.\u201d The first generation father is affected and is labeled \u201c1.\u201d The first generation mother is unaffected and is labeled \u201c2.\u201d The Art Connection question asks the genotype of the three numbered individuals.\" width=\"544\" height=\"478\" \/><\/p>\n<p id=\"caption-attachment-1448\" class=\"wp-caption-text\">Figure\u00a03. In this pedigree analysis for alkaptonuria, individuals with the disorder are indicated in blue and have the genotype aa. Unaffected individuals are indicated in yellow and have the genotype AA or Aa.<\/p>\n<\/div>\n<p>Alkaptonuria is a recessive genetic disorder in which two amino acids, phenylalanine and tyrosine, are not properly metabolized. Affected individuals may have darkened skin and brown urine, and may suffer joint damage and other complications. Looking at Figure\u00a03, we can see that it is often possible to determine a person\u2019s genotype from the genotype of their offspring. For example, if neither parent has the disorder but their child does, they must be heterozygous. Two individuals on the pedigree have an unaffected phenotype but unknown genotype. Because they do not have the disorder, they must have at least one normal allele, so their genotype gets the \u201c<em>A?<\/em>\u201d designation.<\/p>\n<p>What are the genotypes of the individuals labeled 1, 2 and 3?<\/p>\n<\/div>\n<h2>Alternatives to Dominance and Recessiveness<\/h2>\n<p>Mendel\u2019s experiments with pea plants suggested that: (1) two \u201cunits\u201d or alleles exist for every gene; (2) alleles maintain their integrity in each generation (no blending); and (3) in the presence of the dominant allele, the recessive allele is hidden and makes no contribution to the phenotype. Therefore, recessive alleles can be \u201ccarried\u201d and not expressed by individuals. Such heterozygous individuals are sometimes referred to as \u201ccarriers.\u201d Further genetic studies in other plants and animals have shown that much more complexity exists, but that the fundamental principles of Mendelian genetics still hold true. In the sections to follow, we consider some of the extensions of Mendelism. If Mendel had chosen an experimental system that exhibited these genetic complexities, it\u2019s possible that he would not have understood what his results meant.<\/p>\n<h3>Incomplete Dominance<\/h3>\n<div id=\"attachment_1449\" style=\"width: 360px\" class=\"wp-caption alignright\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1449\" class=\"wp-image-1449\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184218\/Figure_12_02_04.jpg\" alt=\"Photo is of a snapdragon with a pink flower.\" width=\"350\" height=\"466\" \/><\/p>\n<p id=\"caption-attachment-1449\" class=\"wp-caption-text\">Figure\u00a04. These pink flowers of a heterozygote snapdragon result from incomplete dominance. (credit: \u201cstorebukkebruse\u201d\/Flickr)<\/p>\n<\/div>\n<p>Mendel\u2019s results, that traits are inherited as dominant and recessive pairs, contradicted the view at that time that offspring exhibited a blend of their parents\u2019 traits. However, the heterozygote phenotype occasionally does appear to be intermediate between the two parents. For example, in the snapdragon, <em>Antirrhinum majus<\/em> (Figure), a cross between a homozygous parent with white flowers (<em>C<sup class=\"sup\">W<\/sup>C<sup class=\"sup\">W<\/sup><\/em>) and a homozygous parent with red flowers (<em>C<sup class=\"sup\">R<\/sup>C<sup class=\"sup\">R<\/sup><\/em>) will produce offspring with pink flowers (<em>C<sup class=\"sup\">R<\/sup>C<sup class=\"sup\">W<\/sup><\/em>). (Note that different genotypic abbreviations are used for Mendelian extensions to distinguish these patterns from simple dominance and recessiveness.) This pattern of inheritance is described as <b>incomplete dominance<\/b>, denoting the expression of two contrasting alleles such that the individual displays an intermediate phenotype. The allele for red flowers is incompletely dominant over the allele for white flowers. However, the results of a heterozygote self-cross can still be predicted, just as with Mendelian dominant and recessive crosses. In this case, the genotypic ratio would be 1 <em>C<sup class=\"sup\">R<\/sup>C<sup class=\"sup\">R<\/sup><\/em>:2 <em>C<sup class=\"sup\">R<\/sup>C<sup class=\"sup\">W<\/sup><\/em>:1 <em>C<sup class=\"sup\">W<\/sup>C<sup class=\"sup\">W<\/sup><\/em>, and the phenotypic ratio would be 1:2:1 for red:pink:white.<\/p>\n<h3>Codominance<\/h3>\n<p>A variation on incomplete dominance is <b>codominance<\/b>, in which both alleles for the same characteristic are simultaneously expressed in the heterozygote. An example of codominance is the MN blood groups of humans. The M and N alleles are expressed in the form of an M or N antigen present on the surface of red blood cells. Homozygotes (<em>L<sup class=\"sup\">M<\/sup>L<sup class=\"sup\">M<\/sup><\/em> and <em>L<sup class=\"sup\">N<\/sup>L<sup class=\"sup\">N<\/sup><\/em>) express either the M or the N allele, and heterozygotes (<em>L<sup class=\"sup\">M<\/sup>L<sup class=\"sup\">N<\/sup><\/em>) express both alleles equally. In a self-cross between heterozygotes expressing a codominant trait, the three possible offspring genotypes are phenotypically distinct. However, the 1:2:1 genotypic ratio characteristic of a Mendelian monohybrid cross still applies.<\/p>\n<h3>Multiple Alleles<\/h3>\n<p>Mendel implied that only two alleles, one dominant and one recessive, could exist for a given gene. We now know that this is an oversimplification. Although individual humans (and all diploid organisms) can only have two alleles for a given gene, multiple alleles may exist at the population level such that many combinations of two alleles are observed. Note that when many alleles exist for the same gene, the convention is to denote the most common phenotype or genotype among wild animals as the <b>wild type<\/b> (often abbreviated \u201c+\u201d); this is considered the standard or norm. All other phenotypes or genotypes are considered <b>variants<\/b> of this standard, meaning that they deviate from the wild type. The variant may be recessive or dominant to the wild-type allele.<\/p>\n<p>An example of multiple alleles is coat color in rabbits (Figure\u00a05). Here, four alleles exist for the <em>c<\/em> gene. The wild-type version, <em>C<sup class=\"sup\">+<\/sup>C<sup class=\"sup\">+<\/sup><\/em>, is expressed as brown fur. The chinchilla phenotype, <em>c<sup class=\"sup\">ch<\/sup>c<sup class=\"sup\">ch<\/sup><\/em>, is expressed as black-tipped white fur. The Himalayan phenotype, <em>c<sup class=\"sup\">h<\/sup>c<sup class=\"sup\">h<\/sup><\/em>, has black fur on the extremities and white fur elsewhere. Finally, the albino, or \u201ccolorless\u201d phenotype, <em>cc<\/em>, is expressed as white fur. In cases of multiple alleles, dominance hierarchies can exist. In this case, the wild-type allele is dominant over all the others, chinchilla is incompletely dominant over Himalayan and albino, and Himalayan is dominant over albino. This hierarchy, or allelic series, was revealed by observing the phenotypes of each possible heterozygote offspring.<\/p>\n<div id=\"attachment_1450\" style=\"width: 810px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1450\" class=\"size-full wp-image-1450\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184300\/Figure_12_02_05.jpg\" alt=\"This illustration shows the four different variants for coat color in rabbits at the c allele. The genotype CC produces the wild type phenotype, which is brown. The genotype c^{ch}c^{ch} produces the chinchilla phenotype, which is black-tipped white fur. The genotype c^{h}c^{h} produces the Himalayan phenotype, which is white on the body and black on the extremities. The genotype cc produces the recessive phenotype, which is white\" width=\"800\" height=\"574\" \/><\/p>\n<p id=\"caption-attachment-1450\" class=\"wp-caption-text\">Figure\u00a05. Four different alleles exist for the rabbit coat color (C) gene.<\/p>\n<\/div>\n<div id=\"attachment_1451\" style=\"width: 360px\" class=\"wp-caption alignright\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1451\" class=\"wp-image-1451\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184330\/Figure_12_02_06.jpg\" alt=\"This photo shows Drosophila that has normal antennae on its head, and a mutant that has legs on its head.\" width=\"350\" height=\"345\" \/><\/p>\n<p id=\"caption-attachment-1451\" class=\"wp-caption-text\">Figure\u00a06. As seen in comparing the wild-type Drosophila (left) and the Antennapedia mutant (right), the Antennapedia mutant has legs on its head in place of antennae.<\/p>\n<\/div>\n<p>The complete dominance of a wild-type phenotype over all other mutants often occurs as an effect of \u201cdosage\u201d of a specific gene product, such that the wild-type allele supplies the correct amount of gene product whereas the mutant alleles cannot. For the allelic series in rabbits, the wild-type allele may supply a given dosage of fur pigment, whereas the mutants supply a lesser dosage or none at all. Interestingly, the Himalayan phenotype is the result of an allele that produces a temperature-sensitive gene product that only produces pigment in the cooler extremities of the rabbit\u2019s body.<\/p>\n<p>Alternatively, one mutant allele can be dominant over all other phenotypes, including the wild type. This may occur when the mutant allele somehow interferes with the genetic message so that even a heterozygote with one wild-type allele copy expresses the mutant phenotype. One way in which the mutant allele can interfere is by enhancing the function of the wild-type gene product or changing its distribution in the body. One example of this is the <em>Antennapedia<\/em> mutation in <em>Drosophila<\/em> (Figure\u00a06). In this case, the mutant allele expands the distribution of the gene product, and as a result, the <em>Antennapedia<\/em> heterozygote develops legs on its head where its antennae should be.<\/p>\n<div class=\"textbox key-takeaways\">\n<h3>Evolution Connection<\/h3>\n<h4>Multiple Alleles Confer Drug Resistance in the Malaria Parasite<\/h4>\n<p>Malaria is a parasitic disease in humans that is transmitted by infected female mosquitoes, including <em>Anopheles gambiae<\/em> (Figure<strong class=\"emphasis\" data-effect=\"bold\">\u00a0<\/strong>7a), and is characterized by cyclic high fevers, chills, flu-like symptoms, and severe anemia. <em>Plasmodium falciparum<\/em> and <em>P. vivax<\/em> are the most common causative agents of malaria, and <em>P. falciparum<\/em> is the most deadly (Figure\u00a07b)<em>.<\/em> When promptly and correctly treated, <em>P. falciparum<\/em> malaria has a mortality rate of 0.1 percent. However, in some parts of the world, the parasite has evolved resistance to commonly used malaria treatments, so the most effective malarial treatments can vary by geographic region.<\/p>\n<div id=\"attachment_1452\" style=\"width: 717px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1452\" class=\"size-full wp-image-1452\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184426\/Figure_12_02_07.png\" alt=\"Photo a shows the Anopheles gambiae mosquito, which carries malaria. Photo b shows a micrograph of sickle-shaped Plasmodium falciparum, the parasite that causes malaria. The Plasmodium is about 0.75 microns across.\" width=\"707\" height=\"326\" \/><\/p>\n<p id=\"caption-attachment-1452\" class=\"wp-caption-text\">Figure\u00a07. The (a) Anopheles gambiae, or African malaria mosquito, acts as a vector in the transmission to humans of the malaria-causing parasite (b) Plasmodium falciparum, here visualized using false-color transmission electron microscopy. (credit a: James D. Gathany; credit b: Ute Frevert; false color by Margaret Shear; scale-bar data from Matt Russell)<\/p>\n<\/div>\n<p>In Southeast Asia, Africa, and South America, <em>P. falciparum<\/em> has developed resistance to the anti-malarial drugs chloroquine, mefloquine, and sulfadoxine-pyrimethamine. <em>P. falciparum<\/em>, which is haploid during the life stage in which it is infectious to humans, has evolved multiple drug-resistant mutant alleles of the <em>dhps<\/em> gene. Varying degrees of sulfadoxine resistance are associated with each of these alleles. Being haploid, <em>P. falciparum<\/em> needs only one drug-resistant allele to express this trait.<\/p>\n<p>In Southeast Asia, different sulfadoxine-resistant alleles of the <em>dhps<\/em> gene are localized to different geographic regions. This is a common evolutionary phenomenon that occurs because drug-resistant mutants arise in a population and interbreed with other <em>P. falciparum<\/em> isolates in close proximity. Sulfadoxine-resistant parasites cause considerable human hardship in regions where this drug is widely used as an over-the-counter malaria remedy. As is common with pathogens that multiply to large numbers within an infection cycle, <em>P. falciparum<\/em> evolves relatively rapidly (over a decade or so) in response to the selective pressure of commonly used anti-malarial drugs. For this reason, scientists must constantly work to develop new drugs or drug combinations to combat the worldwide malaria burden.<a class=\"footnote\" title=\"Sumiti Vinayak, et al., \u201cOrigin and Evolution of Sulfadoxine Resistant Plasmodium falciparum,\u201d Public Library of Science Pathogens 6, no. 3 (2010): e1000830, doi:10.1371\/journal.ppat.1000830.\" id=\"return-footnote-241-1\" href=\"#footnote-241-1\" aria-label=\"Footnote 1\"><sup class=\"footnote\">[1]<\/sup><\/a><\/p>\n<\/div>\n<h2>X-Linked Traits<\/h2>\n<p>In humans, as well as in many other animals and some plants, the sex of the individual is determined by sex chromosomes. The sex chromosomes are one pair of non-homologous chromosomes. Until now, we have only considered inheritance patterns among non-sex chromosomes, or <b>autosomes<\/b>. In addition to 22 homologous pairs of autosomes, human females have a homologous pair of X chromosomes, whereas human males have an XY chromosome pair. Although the Y chromosome contains a small region of similarity to the X chromosome so that they can pair during meiosis, the Y chromosome is much shorter and contains many fewer genes. When a gene being examined is present on the X chromosome, but not on the Y chromosome, it is said to be <b>X-linked<\/b>.<\/p>\n<div id=\"attachment_1453\" style=\"width: 360px\" class=\"wp-caption alignright\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1453\" class=\"wp-image-1453\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184500\/Figure_12_02_08.jpeg\" alt=\"Photo shows six fruit flies, each with a different eye color.\" width=\"350\" height=\"439\" \/><\/p>\n<p id=\"caption-attachment-1453\" class=\"wp-caption-text\">Figure\u00a08. In Drosophila, the gene for eye color is located on the X chromosome. Clockwise from top left are brown, cinnabar, sepia, vermilion, white, and red. Red eye color is wild-type and is dominant to white eye color.<\/p>\n<\/div>\n<p>Eye color in <em>Drosophila<\/em> was one of the first X-linked traits to be identified. Thomas Hunt Morgan mapped this trait to the X chromosome in 1910. Like humans, <em>Drosophila<\/em> males have an XY chromosome pair, and females are XX. In flies, the wild-type eye color is red (X<sup class=\"sup\"><em>W<\/em><\/sup>) and it is dominant to white eye color (X<sup class=\"sup\"><em>w<\/em><\/sup>) (Figure\u00a08). Because of the location of the eye-color gene, reciprocal crosses do not produce the same offspring ratios. Males are said to be <b>hemizygous<\/b>, because they have only one allele for any X-linked characteristic. Hemizygosity makes the descriptions of dominance and recessiveness irrelevant for XY males. <em>Drosophila<\/em> males lack a second allele copy on the Y chromosome; that is, their genotype can only be X<sup class=\"sup\"><em>W<\/em><\/sup>Y or X<sup class=\"sup\"><em>w<\/em><\/sup>Y. In contrast, females have two allele copies of this gene and can be X<sup class=\"sup\"><em>W<\/em><\/sup>X<sup class=\"sup\"><em>W<\/em><\/sup>, X<sup class=\"sup\"><em>W<\/em><\/sup>X<sup class=\"sup\"><em>w<\/em><\/sup>, or X<sup class=\"sup\"><em>w<\/em><\/sup>X<sup class=\"sup\"><em>w<\/em><\/sup>.<\/p>\n<p>In an X-linked cross, the genotypes of F<sub>1<\/sub> and F<sub>2<\/sub> offspring depend on whether the recessive trait was expressed by the male or the female in the P<sub>1<\/sub> generation. With regard to <em>Drosophila<\/em> eye color, when the P<sub>1<\/sub> male expresses the white-eye phenotype and the female is homozygous red-eyed, all members of the F<sub>1<\/sub> generation exhibit red eyes (Figure). The F<sub>1<\/sub> females are heterozygous (X<em><sup class=\"sup\">W<\/sup><\/em>X<em><sup class=\"sup\">w<\/sup><\/em>), and the males are all X<em><sup class=\"sup\">W<\/sup><\/em>Y, having received their X chromosome from the homozygous dominant P<sub>1<\/sub> female and their Y chromosome from the P<sub>1<\/sub> male. A subsequent cross between the X<em><sup class=\"sup\">W<\/sup><\/em>X<em><sup class=\"sup\">w<\/sup><\/em> female and the X<em><sup class=\"sup\">W<\/sup><\/em>Y male would produce only red-eyed females (with X<em><sup class=\"sup\">W<\/sup><\/em>X<em><sup class=\"sup\">W<\/sup><\/em> or X<em><sup class=\"sup\">W<\/sup><\/em>X<em><sup class=\"sup\">w<\/sup><\/em> genotypes) and both red- and white-eyed males (with X<em><sup class=\"sup\">W<\/sup><\/em>Y or X<em><sup class=\"sup\">w<\/sup><\/em>Y genotypes). Now, consider a cross between a homozygous white-eyed female and a male with red eyes. The F<sub>1<\/sub> generation would exhibit only heterozygous red-eyed females (X<em><sup class=\"sup\">W<\/sup><\/em>X<em><sup class=\"sup\">w<\/sup><\/em>) and only white-eyed males (X<em><sup class=\"sup\">w<\/sup><\/em>Y). Half of the F<sub>2<\/sub> females would be red-eyed (X<em><sup class=\"sup\">W<\/sup><\/em>X<em><sup class=\"sup\">w<\/sup><\/em>) and half would be white-eyed (X<em><sup class=\"sup\">w<\/sup><\/em>X<em><sup class=\"sup\">w<\/sup><\/em>). Similarly, half of the F<sub>2<\/sub> males would be red-eyed (X<em><sup class=\"sup\">W<\/sup><\/em>Y) and half would be white-eyed (X<em><sup class=\"sup\">w<\/sup><\/em>Y).<\/p>\n<div class=\"textbox key-takeaways\">\n<h3>Art Connection<\/h3>\n<div id=\"attachment_1454\" style=\"width: 735px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1454\" class=\"size-full wp-image-1454\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184601\/Figure_12_02_09.jpeg\" alt=\"This illustration shows a Punnett square analysis of fruit fly eye color, which is a sex-linked trait. A red-eyed male fruit fly with the genotype X^{w}Y is crossed with a white-eyed female fruit fly with the genotype X^{w}X^{w}. All of the female offspring acquire a dominant W allele from the father and a recessive w allele from the mother, and are therefore heterozygous dominant with red eye color. All of the male offspring acquire a recessive w allele from the mother and a Y chromosome from the father and are therefore hemizygous recessive with white eye color.\" width=\"725\" height=\"729\" \/><\/p>\n<p id=\"caption-attachment-1454\" class=\"wp-caption-text\">Figure\u00a09. Punnett square analysis is used to determine the ratio of offspring from a cross between a red-eyed male fruit fly and a white-eyed female fruit fly.<\/p>\n<\/div>\n<p>What ratio of offspring would result from a cross between a white-eyed male and a female that is heterozygous for red eye color?<\/p>\n<\/div>\n<p>Discoveries in fruit fly genetics can be applied to human genetics. When a female parent is homozygous for a recessive X-linked trait, she will pass the trait on to 100 percent of her offspring. Her male offspring are, therefore, destined to express the trait, as they will inherit their father&#8217;s Y chromosome. In humans, the alleles for certain conditions (some forms of color blindness, hemophilia, and muscular dystrophy) are X-linked. Females who are heterozygous for these diseases are said to be carriers and may not exhibit any phenotypic effects. These females will pass the disease to half of their sons and will pass carrier status to half of their daughters; therefore, recessive X-linked traits appear more frequently in males than females.<\/p>\n<p>In some groups of organisms with sex chromosomes, the gender with the non-homologous sex chromosomes is the female rather than the male. This is the case for all birds. In this case, sex-linked traits will be more likely to appear in the female, in which they are hemizygous.<\/p>\n<h2>Human Sex-linked Disorders<\/h2>\n<p>Sex-linkage studies in Morgan\u2019s laboratory provided the fundamentals for understanding X-linked recessive disorders in humans, which include red-green color blindness, and Types A and B hemophilia. Because human males need to inherit only one recessive mutant X allele to be affected, X-linked disorders are disproportionately observed in males. Females must inherit recessive X-linked alleles from both of their parents in order to express the trait. When they inherit one recessive X-linked mutant allele and one dominant X-linked wild-type allele, they are carriers of the trait and are typically unaffected. Carrier females can manifest mild forms of the trait due to the inactivation of the dominant allele located on one of the X chromosomes. However, female carriers can contribute the trait to their sons, resulting in the son exhibiting the trait, or they can contribute the recessive allele to their daughters, resulting in the daughters being carriers of the trait (Figure\u00a010). Although some Y-linked recessive disorders exist, typically they are associated with infertility in males and are therefore not transmitted to subsequent generations.<\/p>\n<div id=\"attachment_1455\" style=\"width: 665px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1455\" class=\"size-full wp-image-1455\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184635\/Figure_12_02_10.jpeg\" alt=\"A diagram shows an unaffected father with a dominant allele and an unaffected carrier mother with an x-linked recessive allele. Four figures of offspring are shown representing the various resulting genetic combinations: unaffected son, unaffected daughter, affected son, and unaffected carrier daughter.\" width=\"655\" height=\"719\" \/><\/p>\n<p id=\"caption-attachment-1455\" class=\"wp-caption-text\">Figure\u00a010. The son of a woman who is a carrier of a recessive X-linked disorder will have a 50 percent chance of being affected. A daughter will not be affected, but she will have a 50 percent chance of being a carrier like her mother.<\/p>\n<\/div>\n<div class=\"textbox shaded\">\n<h3>Link to Learning<\/h3>\n<p>Watch this video to learn more about sex-linked traits.<\/p>\n<p><iframe loading=\"lazy\" id=\"oembed-1\" title=\"Sex-linked traits | Biomolecules | MCAT | Khan Academy\" width=\"500\" height=\"281\" src=\"https:\/\/www.youtube.com\/embed\/-ROhfKyxgCo?feature=oembed&#38;rel=0\" frameborder=\"0\" allowfullscreen=\"allowfullscreen\"><\/iframe><\/p>\n<\/div>\n<h2>Lethality<\/h2>\n<p>A large proportion of genes in an individual\u2019s genome are essential for survival. Occasionally, a nonfunctional allele for an essential gene can arise by mutation and be transmitted in a population as long as individuals with this allele also have a wild-type, functional copy. The wild-type allele functions at a capacity sufficient to sustain life and is therefore considered to be dominant over the nonfunctional allele. However, consider two heterozygous parents that have a genotype of wild-type\/nonfunctional mutant for a hypothetical essential gene. In one quarter of their offspring, we would expect to observe individuals that are homozygous recessive for the nonfunctional allele. Because the gene is essential, these individuals might fail to develop past fertilization, die <em>in utero<\/em>, or die later in life, depending on what life stage requires this gene. An inheritance pattern in which an allele is only lethal in the homozygous form and in which the heterozygote may be normal or have some altered non-lethal phenotype is referred to as <b>recessive lethal<\/b>.<\/p>\n<p>For crosses between heterozygous individuals with a recessive lethal allele that causes death before birth when homozygous, only wild-type homozygotes and heterozygotes would be observed. The genotypic ratio would therefore be 2:1. In other instances, the recessive lethal allele might also exhibit a dominant (but not lethal) phenotype in the heterozygote. For instance, the recessive lethal <em>Curly<\/em> allele in <em>Drosophila<\/em> affects wing shape in the heterozygote form but is lethal in the homozygote.<\/p>\n<div id=\"attachment_1456\" style=\"width: 310px\" class=\"wp-caption alignright\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1456\" class=\"wp-image-1456\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/198\/2016\/11\/28184712\/Figure_12_02_11.jpeg\" alt=\"Micrograph shows a neuron with nuclear inclusions characteristic of Huntington\u2019s disease.\" width=\"300\" height=\"389\" \/><\/p>\n<p id=\"caption-attachment-1456\" class=\"wp-caption-text\">Figure\u00a011. The neuron in the center of this micrograph (yellow) has nuclear inclusions characteristic of Huntington\u2019s disease (orange area in the center of the neuron). Huntington\u2019s disease occurs when an abnormal dominant allele for the Huntington gene is present. (credit: Dr. Steven Finkbeiner, Gladstone Institute of Neurological Disease, The Taube-Koret Center for Huntington&#8217;s Disease Research, and the University of California San Francisco\/Wikimedia)<\/p>\n<\/div>\n<p>A single copy of the wild-type allele is not always sufficient for normal functioning or even survival. The <b>dominant lethal<\/b> inheritance pattern is one in which an allele is lethal both in the homozygote and the heterozygote; this allele can only be transmitted if the lethality phenotype occurs after reproductive age. Individuals with mutations that result in dominant lethal alleles fail to survive even in the heterozygote form. Dominant lethal alleles are very rare because, as you might expect, the allele only lasts one generation and is not transmitted. However, just as the recessive lethal allele might not immediately manifest the phenotype of death, dominant lethal alleles also might not be expressed until adulthood. Once the individual reaches reproductive age, the allele may be unknowingly passed on, resulting in a delayed death in both generations. An example of this in humans is Huntington\u2019s disease, in which the nervous system gradually wastes away (Figure\u00a011). People who are heterozygous for the dominant Huntington allele (<em>Hh<\/em>) will inevitably develop the fatal disease. However, the onset of Huntington\u2019s disease may not occur until age 40, at which point the afflicted persons may have already passed the allele to 50 percent of their offspring.<\/p>\n<h2>Section Summary<\/h2>\n<p>When true-breeding or homozygous individuals that differ for a certain trait are crossed, all of the offspring will be heterozygotes for that trait. If the traits are inherited as dominant and recessive, the F<sub>1<\/sub> offspring will all exhibit the same phenotype as the parent homozygous for the dominant trait. If these heterozygous offspring are self-crossed, the resulting F<sub>2<\/sub> offspring will be equally likely to inherit gametes carrying the dominant or recessive trait, giving rise to offspring of which one quarter are homozygous dominant, half are heterozygous, and one quarter are homozygous recessive. Because homozygous dominant and heterozygous individuals are phenotypically identical, the observed traits in the F<sub>2<\/sub> offspring will exhibit a ratio of three dominant to one recessive.<\/p>\n<p>Alleles do not always behave in dominant and recessive patterns. Incomplete dominance describes situations in which the heterozygote exhibits a phenotype that is intermediate between the homozygous phenotypes. Codominance describes the simultaneous expression of both of the alleles in the heterozygote. Although diploid organisms can only have two alleles for any given gene, it is common for more than two alleles of a gene to exist in a population. In humans, as in many animals and some plants, females have two X chromosomes and males have one X and one Y chromosome. Genes that are present on the X but not the Y chromosome are said to be X-linked, such that males only inherit one allele for the gene, and females inherit two. Finally, some alleles can be lethal. Recessive lethal alleles are only lethal in homozygotes, but dominant lethal alleles are fatal in heterozygotes as well.<\/p>\n<div class=\"textbox exercises\">\n<h3>Additional Self Check Questions<\/h3>\n<ol>\n<li>In pea plants, round peas (<em>R<\/em>) are dominant to wrinkled peas (<em>r<\/em>). You do a test cross between a pea plant with wrinkled peas (genotype <em>rr<\/em>) and a plant of unknown genotype that has round peas. You end up with three plants, all which have round peas. From this data, can you tell if the round pea parent plant is homozygous dominant or heterozygous? If the round pea parent plant is heterozygous, what is the probability that a random sample of 3 progeny peas will all be round?<\/li>\n<li>What are the genotypes of the individuals labeled 1, 2 and 3?<\/li>\n<li>What ratio of offspring would result from a cross between a white-eyed male and a female that is heterozygous for red eye color?<\/li>\n<li>The gene for flower position in pea plants exists as axial or terminal alleles. Given that axial is dominant to terminal, list all of the possible F<sub>1<\/sub> and F<sub>2<\/sub> genotypes and phenotypes from a cross involving parents that are homozygous for each trait. Express genotypes with conventional genetic abbreviations.<\/li>\n<li>Use a Punnett square to predict the offspring in a cross between a dwarf pea plant (homozygous recessive) and a tall pea plant (heterozygous). What is the phenotypic ratio of the offspring?<\/li>\n<li>Can a human male be a carrier of red-green color blindness?<\/li>\n<\/ol>\n<\/div>\n<div class=\"textbox exercises\">\n<h3>Answers<\/h3>\n<ol>\n<li>You cannot be sure if the plant is homozygous or heterozygous as the data set is too small: by random chance, all three plants might have acquired only the dominant gene even if the recessive one is present. If the round pea parent is heterozygous, there is a one-eighth probability that a random sample of three progeny peas will all be round.<\/li>\n<li>Individual 1 has the genotype <em>aa<\/em>. Individual 2 has the genotype <em>Aa<\/em>. Individual 3 has the genotype <em>Aa<\/em>.<\/li>\n<li>Half of the female offspring would be heterozygous (X<sup class=\"sup\"><em>W<\/em><\/sup>X<sup class=\"sup\"><em>w<\/em><\/sup>) with red eyes, and half would be homozygous recessive (X<sup class=\"sup\"><em>w<\/em><\/sup>X<sup class=\"sup\"><em>w<\/em><\/sup>) with white eyes. Half of the male offspring would be hemizygous dominant (X<sup class=\"sup\"><em>W<\/em><\/sup>Y) withe red yes, and half would be hemizygous recessive (X<sup class=\"sup\"><em>w<\/em><\/sup>Y) with white eyes.<\/li>\n<li>Because axial is dominant, the gene would be designated as <em>A<\/em>. F<sub>1<\/sub> would be all heterozygous <em>Aa<\/em> with axial phenotype. F<sub>2<\/sub> would have possible genotypes of <em>AA<\/em>, <em>Aa<\/em>, and <em>aa<\/em>; these would correspond to axial, axial, and terminal phenotypes, respectively.<\/li>\n<li>The Punnett square would be 2 \u00d7 2 and will have <em>T<\/em> and <em>T<\/em> along the top, and <em>T<\/em> and <em>t<\/em> along the left side. Clockwise from the top left, the genotypes listed within the boxes will be <em>Tt<\/em>, <em>Tt<\/em>, <em>tt<\/em>, and <em>tt<\/em>. The phenotypic ratio will be 1 tall:1 dwarf.<\/li>\n<li>No, males can only express color blindness. They cannot carry it because an individual needs two X chromosomes to be a carrier.<\/li>\n<\/ol>\n<\/div>\n\n\t\t\t <section class=\"citations-section\" role=\"contentinfo\">\n\t\t\t <h3>Candela Citations<\/h3>\n\t\t\t\t\t <div>\n\t\t\t\t\t\t <div id=\"citation-list-241\">\n\t\t\t\t\t\t\t <div class=\"licensing\"><div class=\"license-attribution-dropdown-subheading\">CC licensed content, Shared previously<\/div><ul class=\"citation-list\"><li>Biology. <strong>Authored by<\/strong>: Open Stax. <strong>Project<\/strong>: http:\/\/cnx.org\/contents\/185cbf87-c72e-48f5-b51e-f14f21b5eabd@9.17:1\/Biology. <strong>License<\/strong>: <em><a target=\"_blank\" rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">CC BY: Attribution<\/a><\/em><\/li><\/ul><div class=\"license-attribution-dropdown-subheading\">All rights reserved content<\/div><ul class=\"citation-list\"><li>Sex Linked Traits. <strong>Provided by<\/strong>: Khan Academy. <strong>Located at<\/strong>: <a target=\"_blank\" href=\"http:\/\/youtu.be\/-ROhfKyxgCo\">http:\/\/youtu.be\/-ROhfKyxgCo<\/a>. <strong>License<\/strong>: <em>Other<\/em>. <strong>License Terms<\/strong>: Standard YouTube license<\/li><\/ul><\/div>\n\t\t\t\t\t\t <\/div>\n\t\t\t\t\t <\/div>\n\t\t\t <\/section><hr class=\"before-footnotes clear\" \/><div class=\"footnotes\"><ol><li id=\"footnote-241-1\">Sumiti Vinayak, et al., \u201cOrigin and Evolution of Sulfadoxine Resistant Plasmodium falciparum,\u201d Public Library of Science Pathogens 6, no. 3 (2010): e1000830, doi:10.1371\/journal.ppat.1000830. <a href=\"#return-footnote-241-1\" class=\"return-footnote\" aria-label=\"Return to footnote 1\">&crarr;<\/a><\/li><\/ol><\/div>","protected":false},"author":18,"menu_order":5,"template":"","meta":{"_candela_citation":"[{\"type\":\"copyrighted_video\",\"description\":\"Sex Linked Traits\",\"author\":\"\",\"organization\":\"Khan Academy\",\"url\":\"http:\/\/youtu.be\/-ROhfKyxgCo\",\"project\":\"\",\"license\":\"other\",\"license_terms\":\"Standard YouTube license\"},{\"type\":\"cc\",\"description\":\"Biology\",\"author\":\"Open Stax\",\"organization\":\"\",\"url\":\"\",\"project\":\"http:\/\/cnx.org\/contents\/185cbf87-c72e-48f5-b51e-f14f21b5eabd@9.17:1\/Biology\",\"license\":\"cc-by\",\"license_terms\":\"\"}]","CANDELA_OUTCOMES_GUID":"","pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":[],"pb_section_license":""},"chapter-type":[],"contributor":[],"license":[],"class_list":["post-241","chapter","type-chapter","status-publish","hentry"],"part":231,"_links":{"self":[{"href":"https:\/\/courses.lumenlearning.com\/suny-biology1\/wp-json\/pressbooks\/v2\/chapters\/241","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/courses.lumenlearning.com\/suny-biology1\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/courses.lumenlearning.com\/suny-biology1\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/suny-biology1\/wp-json\/wp\/v2\/users\/18"}],"version-history":[{"count":19,"href":"https:\/\/courses.lumenlearning.com\/suny-biology1\/wp-json\/pressbooks\/v2\/chapters\/241\/revisions"}],"predecessor-version":[{"id":1457,"href":"https:\/\/courses.lumenlearning.com\/suny-biology1\/wp-json\/pressbooks\/v2\/chapters\/241\/revisions\/1457"}],"part":[{"href":"https:\/\/courses.lumenlearning.com\/suny-biology1\/wp-json\/pressbooks\/v2\/parts\/231"}],"metadata":[{"href":"https:\/\/courses.lumenlearning.com\/suny-biology1\/wp-json\/pressbooks\/v2\/chapters\/241\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/courses.lumenlearning.com\/suny-biology1\/wp-json\/wp\/v2\/media?parent=241"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/suny-biology1\/wp-json\/pressbooks\/v2\/chapter-type?post=241"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/suny-biology1\/wp-json\/wp\/v2\/contributor?post=241"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/suny-biology1\/wp-json\/wp\/v2\/license?post=241"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}