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Histone H4K20 methylation mediated chromatin compaction threshold ensures genome integrity by limiting DNA
Muhammad Shoaib1, David Walter1, Peter J Gillespie2
1Biotech Research and Innovation Centre (BRIC), Faculty of Health and Medical Sciences, University of Copenhagen, Ole Maaløes Vej 5, 2200, Copenhagen N, Denmark.
Nature Communications
|September 14, 2018
Summary
Properly organized chromatin after cell division is key for genome stability. This study reveals how SET8-mediated histone methylation controls chromatin compaction, preventing excessive DNA replication and damage in daughter cells.
Area of Science:
- Cell Biology
- Genetics
- Epigenetics
Background:
- Chromatin organization post-mitosis is crucial for genome regulation but not fully understood.
- Mechanisms controlling chromatin structure in daughter cells require elucidation.
Purpose of the Study:
- To investigate the role of chromatin compaction in maintaining genome integrity after mitosis.
- To identify molecular mechanisms controlling chromatin relaxation and replication licensing in early G1 phase.
Main Methods:
- Studied chromatin compaction dynamics upon mitotic exit.
- Investigated the function of SET8 and histone H4 lysine 20 methylation.
- Assessed replication licensing by monitoring origin recognition complex (ORC) and MCM2-7 complex loading.
- Analyzed DNA damage and genome integrity.
Main Results:
- A chromatin compaction threshold post-mitosis limits replication licensing in G1.
- SET8-dependent H4K20 methylation regulates chromatin relaxation.
- Loss of SET8 or H4K20 leads to excessive chromatin decompaction and ORC overloading.
- ORC overloading results in MCM2-7 recruitment, single-stranded DNA formation, and DNA damage.
Conclusions:
- Fine-tuned chromatin relaxation suppresses detrimental replication licensing.
- SET8-mediated H4K20 methylation is essential for maintaining genome integrity during the mitosis-to-G1 transition.
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