Both genetic and nongenetic factors cause the congenital skeletal abnormality known as clubfoot, which occurs with a worldwide incidence of about 1 in 1000 births. Gurnett et al. identified a family in which clubfoot occurred as an autosomal dominant trait due to a mutation in the PITXI gene. DNA testing revealed that 11 people in the family carried the PITXI mutation, but only eight of these people had clubfoot. Calculate the penetrance of the PITXI mutation in this family.
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- One particularly useful feature of the Hardy-Weinberg equation is that it allows us to estimate the frequency of heterozygotes for recessive genetic diseases, assuming that Hardy-Weinberg equilibrium exists. As an example, let’s consider cystic fibrosis, which is a human genetic disease involving a gene that encodes a chloride transporter. Persons with this disorder have an irregularity in salt and water balance. One of the symptoms is thick mucus in the lungs that can contribute to repeated lung infections. In populations of Northern European descent, the frequency of affected individuals is approximately 1 in 2500. Because this is a recessive disorder, affected individuals are homozygotes. Assuming that the population is in Hardy-Weinberg equilibrium, what is the frequency of individuals who are heterozygous carriers?In mice, the trait for high cholesterol is specified by a dominant allele designatedHC, whereas the wild-type allele for normal cholesterol levels is designated hc.Black fur is specified by a recessive allele designated bl, whereas the wild-typeallele which gives brown fur is designated BL. The genes for both of these traitsare 30cM apart on the same autosome. A brown female (#1) with high cholesterolis mated to a black male (#2) with normal cholesterol. The progeny from this crossinclude a brown male (#3) with high cholesterol and a black female (#4) withnormal cholesterol. Mouse #3 is mated to a brown female (#5) with normalcholesterol. If 4 mice are produced from this cross, what is the probability that all 4will have brown fur?In the 1800s, a man with dwarfism who lived in Utah produced a large number of descendants: 22 children, 49 grandchildren, and 250 greatgrandchildren (see the illustration of a family pedigree to the right), many of whom also exhibited dwarfism (F. F. Stephens. 1943. Journal of Heredity 34:229–235). The type of dwarfism found in this family is called Schmid-type metaphyseal chondrodysplasia, although it was originally thought to be achondroplastic dwarfism. Among the families of this kindred, dwarfism appeared only in members who had one parent with dwarfism. When one parent exhibited dwarfism, the following numbers of children were produced. Q. Use chi-square tests to determine if the numbers of children with each phenotype in family C (1 with normal stature, 6 with dwarfism) and in family D (6 with normal stature, 2 with dwarfism) are significantlydifferent from the numbers expected on the basis of your proposed mode of inheritance. How would you explain these deviations from the…
- Until very recently, the fitness of an individual getting familial retinoblastoma was zero, and if the frequency of babies with the inherited disease is 1/20000, what is the best estimate of the mutation rate of the wild type allele to the non-functional form?Take the example of B-thalassemia, an autosomal recessive genetic disease that particularly affects people from around the Mediterranean. This disease is associated with an anomaly of hemoglobin, a protein essential for the transport of oxygen, which is composed of four chains: two alpha (a) and two beta (B). In case of B-thalassemia, the ẞ chains are produced in insufficient or no quantity in an individual homozygous recessive resulting in insufficient production of overall hemoglobin leading to anemia and other physiological challenges. The gene that controls the synthesis of the ẞ chains is located on chromosome 11. Here is part of the coding portion of this gene (which controls a total of 146 amino acids and of which you only see the portion 36 to 41) and one of the targeted mutations: 1. Give the sequence of amino acids from the template and mutated strands. 2. What type of point mutation is it? 3. Using the principles of the theory of evolution, explain briefly and generally why…Many genetic disorders exhibit locus heterogeneity. Define andgive two examples of locus heterogeneity. How does locus heterogeneityconfound a pedigree analysis?
- A DNA variant has been found linked to a rare autosomal dominant disease in humans and can thus beused as a marker to follow inheritance of the diseaseallele. In an informative family (in which one parentis heterozygous for both the disease allele and the DNA marker in a known chromosomal arrangementof alleles, and his or her mate does not have the samealleles of the DNA variant), the reliability of such amarker as a predictor of the disease in a fetus is related to the map distance between the DNA markerand the gene causing the disease.Imagine that a man affected with the disease(genotype Dd) is heterozygous for the V1and V2forms of the DNA variant, with form V1on the samechromosome as the D allele and form V2on the samechromosome as d. His wife is V3V3dd, where V3isanother allele of the DNA marker. Typing of the fetusby amniocentesis reveals that the fetus has the V2andV3variants of the DNA marker. How likely is it thatthe fetus has inherited the disease allele D if thedistance…A study of SNPs associated with familial hypercholesterolemia has revealed that 7 or more contributing alleles at 6 loci can lead to elevated levels of cholesterol in the blood. What is the probability that the following parents, AaBbccDDeeFF x AAbbCCDdEeFF, will have children that are susceptible to hypercholesterolemia?The gene controlling ABO blood type and the gene underlying nail-patella syndrome are said to show linkage. What does that mean in terms of their relative locations in the genome? What does it mean in terms of how the two traits are inherited with respect to each other?
- As it turned out, one of the tallest Potsdam Guards had an unquenchable attraction to short women. During his tenure as guard, he had numerous clandestine affairs. In each case, children resulted. Subsequently, some of the childrenwho had no way of knowing that they were relatedmarried and had children of their own. Assume that two pairs of genes determine height. The genotype of the 7-foot-tall Potsdam Guard was A9A9B9B9, and the genotype of all of his 5-foot clandestine lovers was AABB. An A9 or B9 allele in the offspring each adds 6 inches to the base height of 5 feet conferred by the AABB genotype. a. What were the genotypes and phenotypes of all the F1 children? b. Diagram the cross between the F1 offspring, and give all possible genotypes and phenotypes of the F2 progenya. If an individual who is homozygous for the mutation found in individual 2 and heterozygous for the mutation found in individual 4 marries an individual who is homozygous for the mutation found in individual 4 and heterozygous for the mutation found in individual 2, what will be the phenotype of their children? b. List the intermediate that would build up in each of the types of children who could not produce protein E.In a study of a muscle disorder, several affected families exhibited vision problems, muscle weakness, and deafness (M. Zeviani et al. 1990. American Journal of Human Genetics 47:904–914). Analysis of the mtDNA from affected members of these families revealed that large numbers of their mtDNA molecules possessed deletions of varying lengths. Different members of the same family and even different mitochondria from the same person possessed deletions of different sizes, so the underlying defect appeared to be a tendency for the mtDNA of affected persons to have deletions. A pedigree of one of the families studied is shown below. The researchers concluded that this disorder is inherited as an autosomal dominant trait, and they mapped the diseasecausing gene to a position on chromosome 10 in the nucleus. Q. Explain how a mutation in a nuclear gene might lead to deletions in mtDNA.