Sarah's Assignment

I'm interested in the DNA repair mechanisms our species might have. Since or species is in such exposed conditions, how does it evade the mutational effects of UV light?

Commonly found UV-mediated mutations are cyclobutane dimers (pyrimidine dimers) and 6-4 photodimers.

Cyclobutane dimers consist of either C=C binding or T=T binding. UV light creates covalent bonds between adjacent thymidines or cytosines,which can inhibit transcription or replication of DNA. Cytosines that are part of a dimer are also more likely to be deaminated and changed to uracil. This can cause errors in either transcription or replication [1] [2].

Deoxyribodipyrimidine photolyases are partially responsible for correcting cyclobutane dimers by breaking the covalent bonds formed by UV light exposure. The reaction they perform can be characterized by: cyclobutadipyrimidine (in DNA) = 2 pyrimidine residues (in DNA) [3]. Interestingly, these photolysases are not found in placental mammals.

Our species has a deoxyribodipyrimidine photolyase-related protein (644030931) which is light dependent. SInce mutations from UV light are more likely to occur during the day, it stands to reason that the repair mechanism would be light-dependent and function only when necessary.