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Non-enzymatic Roles of Human RAD51 at Stalled Replication Forks

Non-enzymatic Roles of Human RAD51 at Stalled Replication Forks

Jennifer M Mason, Yuen-Ling Chan, Ralph W Weichselbaum, Douglas K Bishop

Nat Commun. 2019 Sep 27;10(1):4410.

PMID: 31562309

Abstract:

The central recombination enzyme RAD51 has been implicated in replication fork processing and restart in response to replication stress. Here, we use a separation-of-function allele of RAD51 that retains DNA binding, but not D-loop activity, to reveal mechanistic aspects of RAD51's roles in the response to replication stress. Here, we find that cells lacking RAD51's enzymatic activity protect replication forks from MRE11-dependent degradation, as expected from previous studies. Unexpectedly, we find that RAD51's strand exchange activity is not required to convert stalled forks to a form that can be degraded by DNA2. Such conversion was shown previously to require replication fork regression, supporting a model in which fork regression depends on a non-enzymatic function of RAD51. We also show RAD51 promotes replication restart by both strand exchange-dependent and strand exchange-independent mechanisms.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42414968	RAD51 human			Price

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