Replication stress induces the formation of transient chromatin loops that enclose de novo heterochromatin-enriched stalled replication forks.

Nature Communications - Replication fork plasticity upon genotoxic stress is modulated by nuclear architectural components by elusive mechanisms. Here the authors implicate Lamin A/C – best...

Using biochemical assays and a mutant disrupting RNF168-dependent ubiquitination of the histone variant macroH2A1.2, Galloy et al. identified an unexpected role for histone mH2A1.2 ubiquitination in p...

Lamin A/C maintains replication fork integrity during mild replication stress by modulating chromatin structure and restraining RECQ1 activity.

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Mild replication interference is a consolidated strategy for cancer chemotherapy. Tolerance to mild replication stress (RS) relies on active fork slowing, mediated by transient fork reversal and RECQ1...

By developing a long-read sequencing method to simultaneously map replication status and protein-DNA contacts in cells, Ostrowski, Yang, et al. show that newly replicated chromatin is enriched for unw...

Feng et al. uncover a critical genetic interaction between the DNA translocases SMARCAL1 and FANCM. Their combined loss leads to catastrophic genome instability, particularly at simple-repeat sequence...

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