Reference - PMID:31262821 - Replication fork stalling elicits chromatin compaction for the stability of stalling replication forks.
Reference summary
- PubMed ID
- PMID:31262821
- Title
- Replication fork stalling elicits chromatin compaction for the stability of stalling replication forks.
- Authors
- Feng G, Yuan Y, Li Z, Wang L, Zhang B, Luo J, Ji J, Kong D
- Citation
- Proc Natl Acad Sci U S A 2019 Jul 16;116(29):14563-14572
- Publication year
- 2019
- 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.
