Steven Frank and Laurence Hurst argued that a cytoplasmically inherited mutation in humans that has severe effects in males but no effect in females will not be eliminated from a population by natural selection because only females pass on mtDNA. Using this argument, explain why males with Leber hereditary optic neuropathy are more severely affected than females.

Steven Frank and Laurence Hurst argued that a cytoplasmically inherited mutation in humans that has severe effects in males but no effect in females will not be eliminated from a population by natural selection because only females pass on mtDNA. Using this argument, explain why males with Leber hereditary optic neuropathy are more severely affected than females.

Biology (MindTap Course List)

11th Edition

ISBN:9781337392938

Author:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. Berg

Publisher:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. Berg

Chapter19: Evolutionary Change In Populations

Section: Chapter Questions

Problem 15TYU

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Steven Frank and Laurence Hurst argued that a cytoplasmically inherited mutation in humans that has severe effects in males but no effect in females will not be eliminated from a population by natural selection because only females pass on mtDNA (S. A. Frank and L. D. Hurst. 1996. Nature 383:224). Using this argument, explain why males with Leber hereditary optic neuropathy are more severely affected than females.
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. What characteristics of the pedigree rule out inheritance of a trait encoded by a gene in the mtDNA as the cause of this disorder?
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.
Malaria is a leading cause of human illness and mortality worldwide, with 200 million people infected and 600,000 deaths each year. In the 1960s, the incidence of malaria was reduced owing to the use of insecticides that killed mosquitoes in the genus Anopheles, which transmit the disease from person to person. But today, mosquitoes are becoming resistant to insecticides--causing a resurgence in malaria. In this exercise, you will investigate whether alleles encoding resistance to insecticides have been transferred between closely related species of Anopheles. To find out whether transfers have occurred, you will analyze DNA results from two species of mosquitoes that transmit malaria (Anopheles gambiae and A. coluzzii) and from A. gambiae × A. coluzzii hybrids. Resistance to DDT and other insecticides in Anopheles is affected by a sodium channel gene, kdr. The allele r of this gene confers resistance, while the wild type (+/+) genotype is not resistant. Researchers sequenced the kdr…
Suppose we define the Alzheimer's disease phenotype as being diagnosed with the disease by age 75 years. In the human population, there are three alleles of the ApoE gene: e2, e3, e4. They form an allelic series such that: 70% of 75 year olds with the e4/e4 genotype have the Alzheimer's phenotype 60% of 75 year olds with the e3/e4 genotype have the Alzheimer's phenotype 40% of 75 year olds with the e3/e3 genotype have the Alzheimer's phenotype 30% of 75 year olds with the e2/e4 genotype have the Alzheimer's phenotype 10% of 75 year olds with the e2/e3 genotype have the Alzheimer's phenotype If I have the e4/e4 genotype and my wife has the e2/e3 genotype, what is the probability that our child will have Alzheimer's by age 75. Explain your reasoning.
In a study of a muscle disorder, several affected families exhibitedvision problems, muscle weakness, and deafness (M. Zeviani et al. 1990.American Journal of Human Genetics 47:904–914). Analysis of themtDNA from affected members of these families revealed that largenumbers of their mtDNA molecules possessed deletions of varyinglengths. Different members of the same family and even differentmitochondria from the same person possessed deletions of differentsizes, so the underlying defect appeared to be a tendency for the mtDNAof affected persons to have deletions. A pedigree of one of the familiesstudied is shown below. The researchers concluded that this disorder isinherited as an autosomal dominant trait, and they mapped the diseasecausinggene to a position on chromosome 10 in the nucleus.a. What characteristics of the pedigree rule out inheritance of a traitencoded by a gene in the mtDNA as the cause of this disorder?b. Explain how a mutation in a nuclear gene might lead to deletions…
Suppose we define the Alzheimer’s disease phenotype as being diagnosed with the disease by age 75 years. In the human population, there are three alleles of the ApoE gene: ε2, ε3, ε4. They form an allelic series such that: 70% of 75 year olds with the ε4/ ε4 genotype have the Alzheimer’s phenotype 60% of 75 year olds with the ε3/ ε4 genotype have the Alzheimer’s phenotype 40% of 75 year olds with the ε3/ ε3 genotype have the Alzheimer’s phenotype 30% of 75 year olds with the ε2/ ε4 genotype have the Alzheimer’s phenotype 10% of 75 year olds with the ε2/ ε3 genotype have the Alzheimer’s phenotype If I have the ε4/ ε4 genotype and my wife has the ε2/ ε3 genotype, what is the probability that our child will have Alzheimer’s by age 75. Explain your reasoning. [Can be answered in less than 75 words]
In recent years, the country of Zambia in Africa has had increasing cases of malaria. If 8 % of the population is born with a severe form of sickle-cell anemia (ss), what percentage of the population will be more resistant to malaria because they are heterozygous (Ss) for the sickle-cell gene, under the Hardy-Weinberg assumption?
I have seen that this was answered as C, Why is the answer C, how is that not evidence of it being genetic? Shouldnt it be none of the above? Question: Of the following, which supports the idea that alcoholism has no genetic or a low genetic component? a) Some strains of mice select alcohol over water 75% of the time, whereas others shun alcohol. b) The concordance value is 55% for MZ twins and 28% for DZ twins. c) Biological sons of alcoholic men who have been adopted have a rate of alcoholism more like that of their adoptive fathers. d) There is a 20% to 25% risk of alcoholism in the sons of alcoholic men. e) None of these.
The agouti gene determines coat colour in mice. Heterozygous mice have yellow coats, while homozygous dominant mice have black coats. However, having two copies of the recessive alleles is lethal. In a population of 2 000 mice, 1 082 mice have black coats. a) Calculate the frequency of each allele. Show all your work and express your answer as a value between 0 and 1 rounded to two decimal places. b) What percentage of the mouse population is expected to be carriers of the lethal allele? Show all your work and express your answer rounded to one decimal place. c) How many mice will die during fetal development? Show all your work and round your answer to the closest whole number.
The mutation rate of the genome of SARS-COV2 is estimated to be between 0.8-2.38 x 103. Let's use the mutation rate of 0.0008 of a particular site converting allele A2 to A1 (careful with this one). Let's imagine that the initial allele frequencies are: A1 = 0.8 = p %3D A2 = 0.2 = q What is the allele frequency of allele A1 in the next generation? Please use five decimal points (Using fewer decimals will result in no points for this question).
Some individuals in a canine population is susceptible to disease X, which strikes the adults. The susceptibility is later found to be determined by a single locus, with the R allele dominant over the r allele, such that the rr individuals are susceptible to the disease and the others immune. A population genetic survey showed that 1% of the newborns carry the rr genotype. Also, an independent estimation showed that mutation rate converting R to r is 5 × 10-3 per generation. You suspected that the r allele frequency is maintained by mutation- selection balance (MSB). If your hypothesis of MSB is true, then what is the survival rate for the rr adults? (Note: the equilibrium allele frequency ĝ is calculated as ĝ where %3D u is the mutation rate and s is the selection coefficient.) 5% 50% 95% 99% None of the above