a. How many generations are presented in this pedigree? b. What are the most probable genotype of III-3, II-5, and III-8? c. What is the probability that II- 1 and ll-2 will have another normal offspring? Show punnet square and explain your answer. d. Who among the individuals are affected?
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- Use the pedigree to answer the questions that follow. Make sure you put your answer in the correct blank. A) AB В 1 5 II A A AB B A AB A 3 5 6 7 8 II A A B 2 3 5 6 a) State the possible blood type(s) of individual I-4 b) State the possible blood type(s) of individual I-6 c) State the possible genotype(s) of individual Il-5 d) State the possible genotype(s) of individual II-6 e) Determine the percentage chance that couple Il-4 and Il-5 have another child that has type O blood 2.A. Look at the pedigree, and DISREGARD individual II-8 for the moment. Is the pattern of inheritance of Unetan syndrome dominant or recessive? You may assume that the gene is FULLY-PENETRANT in this family. Please give two specific reasons that support your conclusion. B. Now, looking at BOTH the pedigree AND at the Southern blot, is this trait autosomal, X-linked, or Y-linked? Please give two specific reasons that support your conclusion. Once again, disregard II-8 for the moment. One of your two reasons must refer specifically to evidence present in the Southern blot. C. Define the gene alleles associated with Unetan syndrome. Your alleles MUST be consistent with the pattern of inheritance, AND your genetic notation must be consistent with that used throughout the course. Unetan syndrome allele: ________ Normal allele: ________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…
- Considering the genetics cross andobserved phenotypes pictured:a. Which genetic cross(es) led to themost number of healthy progeny?b. What type of model organism islikely being used in these experiments?c. Explain what is likely causing the embryonic lethality based on the observed percentages of embryoniclethality.d. What form of genetic material (maternal, paternal, or both) is leading to the embryonic lethalphenotype?e. Why do you think the second bar has the highest “n” number? What does the “n” value indicate?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?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?
- 1. The pedigree below shows the incidence of rare, autosomal dominant disorder called Ehlers-Danlos disease. The pedigree covers three generations of a particular family and also shows individual genotypes at a potential marker locus (M). a) Indicate the phase of all gen II and III individuals. DdM1M3 ddM2M6 II DDM3M6 ddM4M5 III DdMзM4 DdMЗМ5 DDM3M4 ddM3M5 DDM3M4 ddM5M6 DDM3M4 ddM4M6 ddM5M6 ddM5M6 b) Which, if any, of the gen III individuals are recombinants? c) Calculate the LOD score as a test of physical linkage between the marker (M) and the disease locus. d) What do you conclude about linkage between D and M?Please consider the pedigree below. There are no cases of false paternity. I II III IV в 1 a. Which individual/s definitely has/have Bombay phenotype in the descendants of I-1 and I-2? b. What are the genotypes of individuals II-2 and III-2 at the AB0 and H loci? Please label your answers a and b, Il-2: and Ill-2:.Using designations "Group A", “Group B," etc., organize the mutant strains into complementation groups. If the result of any cross does not fit your groupings, indicate which cross(es) you have excluded. Consider the consequence if one of the mutations was dominant. You should see that complementation tests could not be used to provide information about dominant mutations. a) If a mutation were dominant, how would the diploid be affected? What effect would this have on the determination of your complementation groups? b) How would you test if any of these trp¯ mutations were dominant?
- The XG locus on the human X chromosome has twoalleles, XG+ and XG. The XG+ allele causes the presence of the Xg surface antigen on red blood cells,while the recessive XG allele does not allow antigento appear. The XG locus is 10 m.u. from the STSlocus. The STS+ allele produces normal activity ofthe enzyme steroid sulfatase, while the recessive STSallele results in the lack of steroid sulfatase activityand the disease ichthyosis (scaly skin). A man withichthyosis and no Xg antigen has a normal daughterwith Xg antigen. This daughter is expecting a child.a. If the child is a son, what is the probability he willlack Xg antigen and have ichthyosis?b. What is the probability that a son would have boththe antigen and ichthyosis?c. If the child is a son with ichthyosis, what is theprobability he will have Xg antigen?. A diploid strain of yeast was made by mating a haploidstrain with a genotype w−, x−, y−, and z− with a haploidstrain of opposite mating type that is wild type for thesefour genes. The diploid strain was phenotypically wildtype. Four different X-ray-induced diploid mutantswith the following phenotypes were produced fromthis diploid yeast strain. Assume a single new mutation is present in each strain.Strain 1 w− x+ y− z+Strain 2 w+ x− y− z−Strain 3 w− x+ y− z−Strain 4 w− x+ y+ z+When these mutant diploid strains of yeast go throughmeiosis, each ascus is found to contain only two viablehaploid spores.a. What kind of mutations were induced by X-rays tomake the listed diploid strains?b. Why did two spores in each ascus die?c. Are any of the genes w, x, y, or z located on thesame chromosome?d. Give the order of the genes that are found on thesame chromosomeEnsure answers are clearly labelled a) & b). a) Consider the following pedigree. The solid symbols represent affected individuals. Which of the following is / are possible genotypes for II-2 with respect to this disease? Please type 1 - 4, and indicate yes or no only for each. II III 1. xAxa 2. xaxa 3. Aa 4. AA2 b) Genes A, B and C are on the same chromosome linked in cis (coupling) conformation. A'is 16 cM from B, and B is 22 cM from C. The distance between A and C is 38 cM. The coefficient of coincidence is 0.55 for a trihybrid test cross. How many individuals with the genotype AabbCc do you expect to see among the offspring of the cross if 1000 offspring are obtained? Please show your calculations and round your answer off to the nearest whole number.