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lambert, s.

Publications and source records attributed to lambert, s..

2 recordsLinked to original sources

Vimentin networks at high strains

The cytoskeleton is crucial in maintaining cell shape and structural integrity. It consists of three types of filaments, including actin filaments and intermediate filaments (IFs) that exhibit distinctly different force-strain behavior: while IFs show nonlinear behavior with exceptional extensibility and remarkable resistance against rupture at high strains, actin filaments break at low strains. Here we address the question of whether the intriguing mechanical behavior of vimentin IFs translates to the network scale. We apply high strains to in vitro reconstituted networks using optical tweezers and find contrastive behavior for the two cytoskeletal networks: vimentin networks show strain stiffening behavior and respond in an elastic, solid-like manner with high forces opposing the active movement of the beads, whereas actin networks strain soften and fluidize at low forces. Our work highlights the complementary nature of the components of the cytoskeleton, which - in the cell - are partly co-localized and believed to constitute a composite biological material.

biophysics↗

Histone deposition plays an active role in recombination-dependent replication to balance genome2 stability upon replication stress

Replication stress poses a serious threat to genome and epigenome stability. Recombination-Dependent-Replication (RDR) ensures 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 is required for the completion of RDR. Histone deposition prevents joint-molecules from Rqh1-dependent disassembly, a crosstalk contributing to cell survival upon replication stress but channeling RDR towards deleterious events. Asf1 and CAF-1 act in RDR and CAF-1 recruitment to DNA synthesis associated to RDR requires the HR factor Rad52. Our data establish that CAF-1 counteracts Rqh1 activity at sites of replication stress by promoting repair synthesis-coupled histone deposition. 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.

genetics↗