Rad51 recombinase prevents Mre11 nuclease-dependent degradation and excessive PrimPol-mediated elongation of nascent DNA after UV irradiation

摘要: After UV irradiation, DNA polymerases specialized in translesion synthesis (TLS) aid replication. However, it is unclear whether other mechanisms also facilitate the elongation of UV-damaged DNA. We wondered if Rad51 recombinase (Rad51), a factor that escorts replication forks, aids across lesions. found depletion impairs S-phase progression and increases cell death after irradiation. Interestingly, TLS polymerase polη modulate nascent different ways, suggesting irradiation does not exclusively rely on events. In particular, protects synthesized immediately before from degradation avoids excessive Rad51-depleted samples, was limited to first minutes required exonuclease activity double strand break repair nuclease (Mre11). The persistent dysregulation knockdown Mre11, but its activity, PrimPol, with primase activity. By showing crucial contribution DNA, our results reveal an unanticipated complexity regulation templates.