1. If there were only two alleles of TAS2R38 (AVI and PAV) in the human population, what are the possible allelic combinations in diploid cells? 2. For the sake of simplicity, assume that only the amino acids Pro, Ala and Val make up the functioning active site pocket within the taste receptor TAS2R38. Using your knowledge of amino acid properties, describe the environment of the active site. Is it surprising that changing these amino acids to Ala, Val and Iso, respectively, inhibits the receptor from binding PTC?

1. If there were only two alleles of TAS2R38 (AVI and PAV) in the human population, what are the possible allelic combinations in diploid cells? 2. For the sake of simplicity, assume that only the amino acids Pro, Ala and Val make up the functioning active site pocket within the taste receptor TAS2R38. Using your knowledge of amino acid properties, describe the environment of the active site. Is it surprising that changing these amino acids to Ala, Val and Iso, respectively, inhibits the receptor from binding PTC?

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter15: Genomes And Genomics

Section: Chapter Questions

Problem 1QP: The gene controlling ABO blood type and the gene underlying nail-patella syndrome are said to show...

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Question 15: Consider the consequence if one of the mutations you tested for complementation was a dominant mutation. You should see that complementation tests could not be used to provide information about dominant mutations. a) If a mutation were dominant how would your interpretation of the phenotype of the diploid be altered? No change would occur v b) How would you test whether any of these trp mutations were dominant? There is no way to test fc V
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1. In chipmunks, the relationship between genotype and the age at which heart attacks occur is similar to that in squirrels. However, in chipmunks that are homozygous for the normal LDL receptor allele, Fn, only normal receptors are present. Heterozygous chipmunks have a single type of LDL receptor present on the cell surface, but those defective receptors exhibit only 50% of the normal LDL binding capacity. Finally, chipmunks that are homozygous for the defective receptor allele possess receptors with virtually no LDL binding ability. NAME and DEFINE the genetic phenomenon illustrated here.
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?
6). To investigate the genetic control of locomotive behavior in the diploid nematode, Caenorhabditis elegans, eight "wiggly" mutants were isolated, which wiggle in an uncoordinated way rather than smoothly gliding. These eight mutants were crossed together in all possible pairwise combinations, yielding the results summarized in the table above (+ means that all the progeny were wild type, and m means that all the progeny showed the wiggly mutant phenotype). Organize the eight mutations into con lementation groups, each consisting of a group of mutations affecting the same gene. 1 2 3 4 5 6 7 8 1 E N+E 2 3+1 m + m 4 5 + m m E+ + + EE 6 ++E E+ +EE m m + + + + + + + + + m 7 8 ++4 ∞+E +E m m ++ E
Time mapping is performed in a cross involving the genes his,leu, mal, and xyl. The recipient cells are auxotrophic for all fourgenes. After 25 minutes, mating is interrupted, with the resultsin recipient cells shown below. Diagram the positions of thesegenes relative to the origin (O) of the F factor and to one another.(a) 90% are xyl+(b) 80% are mal+(c) 20% are his+(d) None are leu+
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Flies homozygous for recessive null mutations in thesevenless (sev) or bride-of-sevenless (boss) genes have the same mutant phenotype: Every ommatidium(facet) in their eyes lacks photoreceptor cell 7 (R7).The R7 cells enable flies to detect UV light.a. Given that flies normally move toward light, suggest a screening method that would enable you toidentify mutations in additional genes required forR7 determination.b. Would you be able to recover mutations in everygene required for R7 development with yourmethod? Explain.c. How could you tell whether any of the new mutationsyou found in your screen are alleles of sev or boss?d. Suppose you found one recessive mutant allele ofa gene not previously known to be involved in eyedevelopment. How could you use this allele in anew mutagenesis screen to find additional allelesof this gene? Why might you want additional mutant alleles to study the process?