Histone deposition promotes recombination-dependent replication at arrested forks

Julien Hardy, Dingli Dai, Anissia Ait Saada, Ana Teixeira-Silva, Louise Dupoiron, Fatemeh Mojallali, Karine Fréon, Francoise Ochsenbein, Brigitte Hartmann and Sarah Lambert

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Aug 09, 2018
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Received: 24th July 18

Replication stress poses a serious threat to genome and epigenome stability. Recombination-Dependent-Replication (RDR) promotes DNA synthesis resumption from arrested forks. Despite the identification of chromatin restoration pathways during DNA repair processes, crosstalk coupling RDR and chromatin assembly is largely unexplored. Here, we addressed the contribution of chromatin assembly to replication stress in fission yeast. We expressed a mutated histone (H3-H113D) to genetically impair replication-dependent chromatin assembly by destabilizing (H3-H4)2 tetramer. We established that DNA synthesis-dependent histone deposition, by CAF-1 and Asf1, promotes RDR by preventing Rqh1-mediated disassembly of joint molecules. This crosstalk contributes to cell survival upon replication stress but favors deletion type events. The recombination factor Rad52 is required for CAF-1 binding to the chromatin upon replication stress and to repair-synthesis during RDR. These results demonstrate that histone deposition plays an active role in fine-tuning RDR, a benefit counterbalanced by stabilizing at-risk joint molecules for genome stability.

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This is an abstract of a preprint hosted on an independent third party site. It has not been peer reviewed but is currently under consideration at Nature Communications.

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