If this mistake isnt fixed before replication the

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Unformatted text preview: t shorter each time cells divide, and eventually they enter senescence ­ ­> arrest of cell cycle. Then two things can happen: cells can either enter crisis and die; or they can bypass the crisis and hyperproliferate, i.e. become tumor cells. This is another reason telomerase is implicated in cancer, because tumor cells tend to reactivate their telomerase activity. Repair pathways 1. Direct repair:  ­ ­> not versatile  ­ ­> highly efficient because it fixes specific base modification  ­ ­> good for common mistakes such as O6meG; in this case it’s worth it to have a specific enzyme since you are at risk of converting a GC base pair to a GT base pair. If this mistake isn’t fixed before replication, the information could be changed forever 2. Base excision repair (BER): specific enzymes are glycosylase and AP endonuclease  ­ ­> relatively versatile because it fixes deamination (example: C  ­> U), depurination and depyramidination, which occur spontaneously all the time in cells.  ­ ­> one strand is saved as a template  ­ ­> either starts with an abasic site from depurination/depyramidination or needs a glycosylase to get rid of the wrong base; more versatile than direct repair because after a specific glycosylase...
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