u/Formal_Turnover_2599

This question is referencing a statement in the Kaplan Books (and seemingly a few threads in the past in this subreddit which also claim so):

• "DNA Polymerases Beta and Epsilon are important to the process of DNA repair".

From some digging online, it is clear that Beta plays a dominant role in DNA repair processes. However, I'm a bit confused by the inclusion of Epsilon with the exclusion of Delta in this statement.

From online, it seems that DNA polymerase Delta (POLD) is characterizes as having all the functionality of epsilon (if not more) in terms of DNA repair.

One thing I did find online is the polymerase epsilon (POLE) mutations seem to be more commonly associated w/ cancers, but it seems like modern research has very little evidence of exactly why. One source states that bc POLE corrects for mistakes only in DNA synthesized by itself, while POLD corrects for mistakes by alpha, epsilon, or delta, mutations in POLD are more likely to hurt the cancer to a fitness level that is not sustainable for a cancer cell. [1]

> "One possible partial explanation for the relative lack of POLD1 mutations in cancer may be the role for Pol in what has been called ‘proofreading in trans’ (62) or‘extrinsic proofreading’ (63). Pol can proofread DNA synthesis errors made by any of the three replication DNA Pols (, or ε), while Pol ε can only proofread its own replication errors. In addition to this ability to proofread replication errors, Pol exonuclease activity also plays critical roles in mismatch repair(MMR) and Okazaki fragment maturation (64). Mutations that compromise Pol exonuclease activity might thus prove catastrophic during tumor development by allowing the accumulation of mutations from DNA synthesis errors made by all three replication DNA polymerases instead of only failing to correct its own errors. It may then be that POLE and POLD1 mutations arise stochastically at similar rates, but the subsequent reduced fitness and decreased viability of POLD1 mutants give the later appearance of a smaller number of POLD1 tumors." >

Anyone know why its worded like this / what we need to know for the MCAT?

What do you think? Is it possible to maps human DNA mutation considering how this evolved?