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- In addition to Tc1, the C. elegans genome contains otherfamilies of DNA transposons such as Tc2, Tc3, Tc4, andTc5. Like Tc1, their transposition is repressed in thegerm line but not in somatic cells. Predict the behaviorof these elements in the mutant strains where Tc1 is nolonger repressed due to mutations in the RNAi pathway.Justify your answer.When 1 million cells of a culture of haploid yeastcarrying a met− auxotrophic mutation were plated onpetri plates lacking methionine (Met), five coloniesgrew. You would expect cells in which the originalmet− mutation was reversed (by a base change back tothe original sequence) would grow on the media lackingmethionine, but some of these apparent reversions couldbe due to a mutation in a different gene that somehowsuppresses the original met− mutations. How wouldyou be able to determine if the mutations in your fivecolonies were due either to a precise reversion of theoriginal met− mutation or to the generation of a suppressor mutation in a gene on another chromosome?O The lac operon in E.coli encodes enzymes necessary for the breakdown of lactose. For each enzyme (lac Z and lac Y), indicate with a + or-whether or not it is made when there is no lactose or when there is lactose. B-galactosidase (lac Z) No Lactose Permease (lac Y) Lactose Lactose No Lactose Genotype PP0 Z Y/I P*O*Z•Y* I'POCZ Y*/I P* O©Z*Y° P O Z'Y/I P'OʻZ'Y* PP O ZY*/IP*O*Z*Y* IP OCZ Y /I P*O*Z•Y* IPO ZY*/I* P*O©Z*Y• I'PO*Z Y*/IP'O*Z*Y°
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- Explain the effect of one, two or all three introns removal from the Hes7 gene would reduce the delay the production of the unstable Hes7 gene.Of all the genes in the human genome, the ones withthe most characterized Alu insertions are those thatcause hemophilia, including several insertions in thefactor VIII and factor IX genes. Based on this fact, yourcolleague hypothesizes that the Alu element prefers toinsert into these genes. Do you agree? What other reason can you provide that also explains these data?Researchers have successfully used gene therapy toameliorate some human genetic diseases by adding anormal gene copy to cells whose genomes originallyhad only nonfunctional mutant copies of that gene.For example, a form of blindness due to the lack of asingle protein called RPE65 has been reversed byintroduction of a normal RPE65 gene to cells of theretina of adults.a. The success of this gene therapy approach providesus with clues about the role of the RPE65 proteinin the retina. Do you think that RPE65 is neededfor the proper development of the human eye?b. Can you see a potential difficulty in applying this genetherapy approach for diseases like microcephaly?
- You identify a proflavin-generated allele of a genethat produces a 110-amino acid polypeptide ratherthan the usual 157-amino acid protein. After subjectingthis mutant allele to extensive proflavin mutagenesis,you are able to find a number of intragenic suppressorslocated in the part of the gene between the sequencesencoding the N terminus of the protein and the originalmutation, but no suppressors located in the regionbetween the original mutation and the sequencesencoding the usual C terminus of the protein. Whydo you think this is the case?An investigator was interested in studying UAG nonsense suppressor mutations in bacteria. In one speciesof bacteria, she was able to select two different mutants of this type, one in a tRNATyr gene and the otherin a tRNAGln gene, but in a second species, she wasnot able to obtain any such nonsense suppressor mutations, even after very extensive effort. What couldexplain the difference between the two species?After irradiating wild-type cells of Neurospora (a haploid fungus), a geneticist finds two leucine-requiringauxotrophic mutants. He combines the two mutants ina heterokaryon and discovers that the heterokaryon isprototrophic.a. Were the mutations in the two auxotrophs in the samegene in the pathway for synthesizing leucine or in twodifferent genes in that pathway? Explain.b. Write the genotype of the two strains according toyour model.c. What progeny and in what proportions would youpredict from crossing the two auxotrophic mutants?(Assume independent assortment.)