Lecture 7: DNA repair
1. Thymine dimers are one of the frequent targets of DNA repair systems.
a. What is a thymine dimer.
b. How are thymine dimers formed?
c. Why is it important to remove thymine dimers from DNA
d. Describe a method that eliminates thymine dimers without removing and replacing DNA sequences.
e. Describe as many different mechanisms as you can for removal of thymine dimers from DNA.
2. What is excision repair and how does it work?
3. What is mismatch repair and how does it work?
4. 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?
5. 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?
6. How do mutations induced by X rays and ultraviolet radiation tend to differ from each other?
7. Compare the mechanisms used to overcome ultraviolet light-induced damage to DNA in photoreactivation, as opposed to excision repair.
8. 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? (Hint: you may need to go back to the previous lecture to find the nature of the damage done by alkylating agents)
9. Describe the mechanisms that are involved in postreplicative (recombinational) repair.
10. What is error-prone repair and under what conditions is it invoked? How can the existence of an error-prone repair system be justified (beyond the fact that it has been observed to occur)?
11. Describe the roles played by the RecA protein in various cellular responses to DNA damage.
12. What special mechanisms exist for selective repair of the antisense strands of actively transcribed genes. Why is a comparable level of repair not expected for the sense strands?
13. 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.
14. What genetic defect has been associated with Cockayne syndrome in humans.
15. Starting with a wild type bacterial cell, what mutations would you select for in order to obtain a strain that could be used to test for mutagens with maximum sensitivity. (This will require some speculation -- you have not been given a specific answer.)
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