Dataset Information


Replication fork stalling elicits chromatin compaction for the stability of stalling replication forks.

ABSTRACT: DNA replication forks in eukaryotic cells stall at a variety of replication barriers. Stalling forks require strict cellular regulations to prevent fork collapse. However, the mechanism underlying these cellular regulations is poorly understood. In this study, a cellular mechanism was uncovered that regulates chromatin structures to stabilize stalling forks. When replication forks stall, H2BK33, a newly identified acetylation site, is deacetylated and H3K9 trimethylated in the nucleosomes surrounding stalling forks, which results in chromatin compaction around forks. Acetylation-mimic H2BK33Q and its deacetylase clr6-1 mutations compromise this fork stalling-induced chromatin compaction, cause physical separation of replicative helicase and DNA polymerases, and significantly increase the frequency of stalling fork collapse. Furthermore, this fork stalling-induced H2BK33 deacetylation is independent of checkpoint. In summary, these results suggest that eukaryotic cells have developed a cellular mechanism that stabilizes stalling forks by targeting nucleosomes and inducing chromatin compaction around stalling forks. This mechanism is named the "Chromsfork" control: Chromatin Compaction Stabilizes Stalling Replication Forks.


PROVIDER: S-EPMC6642376 | BioStudies | 2019-01-01

REPOSITORIES: biostudies

Similar Datasets

2017-01-01 | S-EPMC5479891 | BioStudies
2008-01-01 | S-EPMC2481305 | BioStudies
2015-01-01 | S-EPMC4511789 | BioStudies
2019-01-01 | S-EPMC6919565 | BioStudies
2011-01-01 | S-EPMC3074140 | BioStudies
2017-01-01 | S-EPMC5438189 | BioStudies
2009-01-01 | S-EPMC2837601 | BioStudies
2018-01-01 | S-EPMC5969565 | BioStudies
2016-01-01 | S-EPMC4855302 | BioStudies
2008-01-01 | S-EPMC2568021 | BioStudies