AsianScientist (Nov. 17, 2014) – Scientists have uncovered a mechanism involved in maintaining genomic stability in times of cellular stress: the addition of a single molecule of ubiquitin to the histone protein H2B. Their results, published in PLoS Genetics, deepen our understanding of the complex process of DNA replication.
DNA replication is the key process for transmission of genetic information; however, a variety of endogenous or exogenous stresses can halt or alter replication, which may result in genomic instability. Aberrant DNA replication results in mutations and chromosome rearrangements that may be associated with human disorders.
A research team led by Dr. Kao Cheng-Fu, an Assistant Research Fellow at the Institute of Cellular and Organismic Biology under Taiwan’s Academia Sinica, together with researchers from several international institutions, recently discovered that a histone modification known as H2B ubiquitylation (H2Bub), plays a role in regulating DNA replication.
They demonstrated that when DNA replication is disturbed, H2Bub promotes chromatin structure stability by slowing down DNA replication and thereby preventing errors, breaks and other adverse consequences. The authors suggest that H2Bub orchestrates both the formation of chromatin formation and the activation of enzymes involved in the regulation of the cell cycle. This coordination helps cells to recover from cellular stress caused by defects in DNA replication.
Dr. Kao said the results of the study prove that histone H2B ubiquitylation is directly involved in regulating activation of the DNA repair checkpoint and the results provide an opportunity to learn more about how cells maintain genome stability.
The article can be found at: Lin et al. (2014) H2B Mono-ubiquitylation Facilitates Fork Stalling and Recovery during Replication Stress by Coordinating Rad53 Activation and Chromatin Assembly.
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Source: Academia Sinica; Photo: Col Ford and Natasha de Vere/Flickr/CC.
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