Human Heredity: Principles and Issues (MindTap Course List)
Human Heredity: Principles and Issues (MindTap Course List)
11th Edition
ISBN: 9781305251052
Author: Michael Cummings
Publisher: Cengage Learning
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Chapter 10, Problem 21QP

Transcriptional regulators are proteins that bind to promoters (the 5′-flanking regions of genes) to regulate their transcription. Assume that a particular transcription regulator normally promotes transcription of gene X, a transport protein. If a mutation makes this regulator gene nonfunctional, would the resulting phenotype be similar to a mutation in gene X itself? Why or why not?

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Let’s suppose a mutation in the glucocorticoid receptor does not prevent the binding of the glucocorticoid hormone to the protein but prevents the ability of the receptor to activate transcription. Make a list of all the possible defects that may explain why transcription cannot be activated.
If a mutation occurred in the pRM promoter that rendered this promoter as ‘nonfunctional and unable to allow for transcription to occur’,  what would be the outcome?
Most eukaryotic promoters have binding sites for several different transcription factors, and the frequency with which transcription is initiated at a promoter depends on the specific combination of transcriptional regulators bound to their binding sites in that promoter. Transcription of the slither gene in garter snakes is regulated by the transcriptional activators Python and Boa and the transcriptional repressor Sidewinder. Each of these proteins has one binding site in the slither promoter; the affinity of Boa for its binding site is 30 times higher than the affinity of Python for its binding site and 6 times higher than the affinity of Sidewinder for its binding site. Under conditions where Sidewinder is 10 times more abundant than Python, and Python is 3 times as abundant as Boa, would you expect transcription of the slither gene to be activated or repressed? Show or briefly explain how/why you predicted the outcome you chose.
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