Chapter 15: Problem 6
Why is a random mutation more likely to be deleterious than beneficial?
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Chapter 15: Problem 6
Why is a random mutation more likely to be deleterious than beneficial?
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DNA damage brought on by a variety of natural and artificial agents elicits a wide variety of cellular responses involving numerous signaling pathways. In addition to the activation of DNA repair mechanisms, there can be activation of pathways leading to apoptosis (programmed cell death) and cell-cycle arrest. Why would apoptosis and cell-cycle arrest often be part of a cellular response to DNA damage?
What is meant by a conditional mutation?
In a bacterial culture in which all cells are unable to synthesize leucine (leu'), a potent mutagen is added, and the cells are allowed to undergo one round of replication. At that point, samples are taken, a series of dilutions is made, and the cells are plated on either minimal medium or minimal medium containing leucine. The first culture condition (minimal medium) allows the growth of only leu' cells, while the second culture condition (minimal medium with leucine added) allows growth of all cells. The results of the experiment are as follows: $$\begin{array}{lcc} \text { Culture Condition } & \text { Dilution } & \text { Colonies } \\ \text { Minimal medium } & 10^{-1} & 18 \\ \text { Minimal medium + leucine } & 10^{-7} & 6 \end{array}$$ What is the rate of mutation at the locus associated with leucine biosynthesis?
Presented here are hypothetical findings from studies of heterokaryons formed from seven human xeroderma pigmentosum cell strains: $$\begin{array}{lccccccc} & X P 1 & X P 2 & X P 3 & X P 4 & X P 5 & X P 6 & X P 7 \\ X P 1 & \- & & & & & & \\ X P 2 & \- & \- & & & & & \\ X P 3 & \- & \- & \- & & & & \\ X P 4 & \+ & \+ & \+ & \- & & & \\ X P S & \+ & \+ & \+ & \+ & \- & & \\ X P 6 & \+ & \+ & \+ & \+ & \- & \- & \\ X P 7 & \+ & \+ & \+ & \+ & \- & \- & - \end{array}$$ These data are measurements of the occurrence or nonoccur- rence of unscheduled DNA synthesis in the fused heterokaryon. None of the strains alone shows any unscheduled DNA synthesis. Which strains fall into the same complementation groups? How many different groups are revealed based on these data? What can we conclude about the genetic basis of XP from these data?
Contrast the various types of DNA repair mechanisms known to counteract the effects of UV radiation. What is the role of visible light in repairing UV- induced mutations?
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