a. The Y axis is the strength of association between prostate cancer and the variant. b. The spike at the end of Chr 6 indicate the presence of a low risk allele for breast cancer. c. There are 6 SNPs that are associated with increased risk for prostate cancer. Od. The low heritability of prostate cancer makes GWAS an excellent tool for understanding prostate cancer risk. e. The X axis represents any loci in the genome with variation.
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- Familial retinoblastoma, a rare autosomal dominant defect, arose in a large family that had no prior history of the disease. Consider the following pedigree (the darkly colored symbols represent affected individuals): a. Circle the individual(s) in which the mutation most likely occurred. b. Is the person who is the source of the mutation affected by retinoblastoma? Justify your answer. c. Assuming that the mutant allele is fully penetrant, what is the chance that an affected individual will have an affected child?An individual has the following genotype. Gene loci (A) and (B) are 15 m.u. apart. What are the correct frequencies of some of the gametes that car be made by this individual? Bl a O A. Ab = 7.5%; AB = 42.5% B. ab = 25%; aB = 50% O C. AB = 7.5%; aB = 42.5% O D. aB = 15%; Ab = F0% E. aB = 70%; Ab = 15% Reset Selection OMark for Review What's This?A normal appearing female infant was identified with a positive newborn screen, linked to chromosome 12. Few years ago, her older sibling had developed profound hypoglycemia, liver failure leading to coma, and subsequent irreparable brain damage, following a viral illness. The sibling was subsequently shown by clinical testing to have the same disorder that this female infant is screened positive for. a. What is the most likely diagnosis? b. What biomarkers would confirm this on the newborn screening process? Describe the mechanism that causes this metabolic defect.
- The drug ivacaftor has recently been developed totreat cystic fibrosis in children with the rare G551Dmutant allele of CFTR.a. Do you think that ivacaftor would be effective onlyin patients homozygous for the G551D mutation,or might it work as well in compound heterozygotes in which one copy of chromosome 7 hadG551D and the other copy a different allele ofCFTR, such as the more prevalent allele ΔF508?(The protein encoded by G551D folds up properlyand inserts into the cell membrane, but is inefficient in chloride ion transport. Ivacaftor increasesthe efficiency of G551D’s ion transport. TheΔF508 protein does not fold up properly and therefore does not get inserted into the cell membrane.)b. Why do you think ivacaftor would be more effectivein children than in older cystic fibrosis patients?c. The scientists who developed ivacaftor had a modelfor cystic fibrosis: a line of cells that grow in culture and that are homozygous for G551D. Thesecells accumulate mucus at their surfaces that…Consider two maize plants:a. Genotype C/cm ; Ac/Ac+, where cm is an unstableallele caused by a Ds insertionb. Genotype C/cm, where cm is an unstable allele causedby Ac insertionWhat phenotypes would be produced and in whatproportions when (1) each plant is crossed with a basepair-substitution mutant c/c and (2) the plant in part a iscrossed with the plant in part b? Assume that Ac and care unlinked, that the chromosome-breakage frequencyis negligible, and that mutant c /C is Ac+.Mutations in the HPRT1 gene in humans result in atleast two clinical syndromes. Consult OMIM (www.omim.org) by querying HPRT1; you will only needto look briefly at the top three hits (files #300322,300323, and 308000).a. What is the full name of the HPRT1 enzyme?b. On which chromosome is the HPRT1 gene located?c. Mutations in HPRT1 are associated with two different syndromes. What are these syndromes? Foreach, answer the following questions: (i) What arethe symptoms associated with the syndrome? (ii) Isthe mutant allele that causes the syndrome dominant, recessive, codominant, or incompletely dominant with respect to the normal allele, or do specialconditions apply? (iii) Is the syndrome associatedwith a loss-of-function or a gain-of-function disease allele? (iv) Does the syndrome display allelicheterogeneity? (v) Does the syndrome display locus heterogeneity? (Note: You do not need to understand everything in the OMIM entries to answerthese questions.)
- 11). This pedigree illustrates a family in which some members have a completely penetrant disease caused by a dominant mutation. This mutation is linked at a distance of 10 map units from a SNP marker with three different alleles (1, 2 and 3). The SNP alleles found in each family member are indicated below each pedigree symbol. It is not yet evident whether the very young individuals labeled A and B will develop the disease. a. What is the probability that individual A will develop the disease? b. What is the probability that individual B will develop the disease? 1,3 2,2 1,2 3,2 O 1,2 3,2 A BConsider two maize plants:a. Genotype C/c m ; Ac/Ac+, where cm is an unstable allele caused by a Ds insertionb. Genotype C/c m, where cm is an unstable allele caused by Ac insertionWhat phenotypes would be produced and in what proportions when (1) each plant is crossed with a basepair-substitution mutant c/c and (2) the plant in part a is crossed with the plant in part b? Assume that Ac and c are unlinked, that the chromosome-breakage frequency is negligible, and that mutant c /C is Ac+.A. Deletion of the SOX9 gene leads to sex reversal resulting in a person with karyotype 46XY being phenotypically Explain the genetic basis for this. B. Describe what would happen to the phenotype of a male with a mutation in the gene encoding SF1? Explain your answer.
- Figure 19-18a shows a plot of P values (represented bythe dots) along the chromosomes of the dog genome.Each P value is the result of a statistical test of association between a SNP and body size. Other than the clusterof small P values near IGF1, do you see any chromosomalregions with evidence for a significant association between a SNP and body size? Explainthis is what i have said about this image so far, what else can be said aswell including the raw count column. " Interpreting the results of an RNA-Seq analysis is pivotal in understanding the underlying genetic mechanisms of diseases such as breast cancer. In this analysis, Figure 1 provides comprehensive data on differentially expressed genes associated with breast cancer. By delving into the provided information, we can gain valuable insights into the molecular landscape of this disease. First focus is on the gene with the highest fold change, EYA4, situated on chromosome 6. With a staggering fold change of 3604.4176, EYA4 exhibits an unprecedented level of overexpression in cancerous cells compared to normal cells. This profound alteration suggests a pivotal role for EYA4 in breast cancer pathogenesis. The log2 fold change of 11.81555 further emphasizes the magnitude of this difference in gene expression. Statistical significance is evident, with an exceptionally low p-value of…Answer the following questions. 1. Construct a map for the genes d,e,f. Assume that: d and e = 3%; e and f = 5%. Give 2 arrangements of the genes/maps. 2. If d and f = 2%, what is the correct arrangement of the genes d,e,f? 3. Consider the fourth gene "g". if g and e = 1.5%, give two possible arrangements. 4. If d and g = 1.5 % give the correct order of the four genes %3D