Revised November 6, 1998

MCDB 2150 Fall 1998 Review Questions


Lecture 26: DNA damage and repair

1. How does the classical definition of a point mutation differ from the most commonly used modern definition. What changes in our understanding of genetics are responsible for the difference?

2. What is a thymine dimer. How is it formed? Describe two ways it can be removed from DNA.

3. What is mismatch repair and how does it work?

4. What is the genetic defect involved in the human genetic disease Xeroderma pigmentosum? What limitations does it place on the lives of individuals who have it?

5. How do mutations induced by X rays and ultraviolet radiation tend to differ from each other?

6. What is the Ames test and how does it work? What is the rationale for using the Ames test to screen for carcinogens? (textbook page 409)

7. What mechanisms are used to distinguish newly made DNA strands from their template strands to be certain that error correction is done on the new strand and not on the template strand when a mismatch is detected?

8. Describe two different types of recessive mutations and explain how they differ from each other.

9. Describe three different types of dominant mutations and explain how they differ from each other.

10. Compare the mechanisms used to overcome ultraviolet light-induced damage to DNA in photoreactivation, as opposed to excision repair.

11. How is damage to DNA that has been caused by alkylating agents repaired? What is the repair process called? What is the first intermediate step in the repair process?

12. What mutational mechanism appears to have given rise to the blood type O allele during human evolution. Discuss whether or not it is appropriate to refer to the type O allele n comtemporary humans as a mutation.

13. What type(s) of mutagenic agent(s) would you employ if you were seeking to generate stable non-reverting recessive mutations? Include in your answer a discussion of why such agents are likely to produce non-reverting mutations.

14. Describe the last line of defense that a bacterial cell has against ultraviolet damage that is not detected and repaired as soon as it occurs.

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