Identification of a protein essential for a major pathway used by human cells to avoid UV- induced DNA damage

Proceedings of the National Academy of Sciences of the United States of America
Ziqiang LiV M Maher

Abstract

When DNA replication stalls at a fork-blocking lesion, cells use damage tolerance pathways to continue replication. One pathway, "translesion synthesis," involves specialized DNA polymerases that can use damaged DNA as a template. Translesion synthesis can result in mutations (i.e., can be error-prone), but it can also be error-free. An alternative pathway has been hypothesized (sometimes called "damage avoidance"), by which cells make temporary use of an undamaged copy of the blocked sequence as a template, i.e., the newly synthesized daughter strand of the sister duplex or the allelic copy. This pathway is error-free. Evidence of the use of the daughter strand of the sister duplex as a template in intact mammalian cells has not been available heretofore. To determine whether hMms2, a ubiquitin-conjugating enzyme-like protein, plays a critical role in such damage avoidance, a human fibroblast cell strain in which both error-prone translesion synthesis and error-free damage avoidance can be detected and quantified simultaneously, and several derivative strains in which expression of hMms2 protein had been eliminated or greatly decreased, were compared for their ability to avoid translesion synthesis past UV(254nm)-induced DNA p...Continue Reading

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