What is unusual about the [psi-] and [PSI+] phenotypes in yeast?
What will be an ideal response?
Ans: These two phenotypes do not result from a genetic difference; in other words, they are not due to the presence of different alleles. Instead, the [psi-] phenotype is due to a "wild-type" Sup35 protein that causes normal termination of translation. The [PSI+] phenotype is due to a conformational change in the Sup35 protein (influenced by other genes) that causes it to aggregate; it then fails to terminate translation. [psi-] / [PSI+] cells are essentially [PSI+] because the presence of abnormally conformed protein converts the normal form into aggregates.
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A. there is a high statistical frequency of specific amino acids within a given secondary structure B. the folding of the protein is based on how the mRNA folds. C. the physical and energetic properties of the DNA influence protein folding. D. knowing what specific codons are used for each amino acid in the protein can help predict its structure.
A suggested explanation that might be true and is subject to testing by further observations is a(n):
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If the copy number of a proto-oncogene is increased by gene duplication then the proto-oncogene has undergone
A. a missense mutation. B. gene amplification. C. a chromosomal translocation. D. retroviral insertion. E. a nonsense mutation.
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