Chapter 14: Problem 4
Why would a mutation in a somatic cell of a multicellular organism not necessarily result in a detectable phenotype?
Chapter 14: Problem 4
Why would a mutation in a somatic cell of a multicellular organism not necessarily result in a detectable phenotype?
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Get started for freeIn this chapter, we focused on how gene mutations arise and how cells repair DNA damage. At the same time, we found opportunities to consider the methods and reasoning by which much of this information was acquired. From the explanations given in the chapter, (a) How do we know that many cancer-causing agents (carcinogens) are also mutagenic? (b) How do we know that certain chemicals and wavelengths of radiation induce mutations in DNA? (c) How do we know that DNA repair mechanisms detect and correct the majority of spontaneous and induced mutations?
Most mutations in a diploid organism are recessive. Why?
It has been noted that most transposons in humans and other organisms are lacated in noncoding regions of the genome regions such as introns, pseudogenes, and stretches of particular types of repetitive DNA. There are several ways to interpret this observation. Describe two possible interpretations. Which interpretation do you favor? Why?
Contrast and compare the mutagenic effects of deaminating agents, alkylating agents, and base analogs.
What genetic defects result in the disorder xeroderma pigmento\(\operatorname{sum}(\mathrm{XP})\) in humans? How do these defects create the phenotypes associated with the disorder?
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