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Graphic illustrates result on DNA replication of loss of HK37me1

The Kouzarides lab find that two enzymes, Set1 and Set2, are responsible for methylation of H3K37, which protects the genome from inappropriate origin licensing and spurious DNA replication.

 

 

Methylation of histone H3 at lysine 37 by Set1 and Set2 prevents spurious DNA replication

Santos-Rosa H et al. (2021) Molecular Cell 81(13): 2793-2807.e8.  DOI: 10.1016/j.molcel.2021.04.021

 

Abstract from the paper

DNA replication initiates at genomic locations known as origins of replication, which, in S. cerevisiae, share a common DNA consensus motif. Despite being virtually nucleosome-free, origins of replication are greatly influenced by the surrounding chromatin state.

Here, we show that histone H3 lysine 37 mono-methylation (H3K37me1) is catalyzed by Set1p and Set2p and that it regulates replication origin licensing. H3K37me1 is uniformly distributed throughout most of the genome, but it is scarce at replication origins, where it increases according to the timing of their firing.

We find that H3K37me1 hinders Mcm2 interaction with chromatin, maintaining low levels of MCM outside of conventional replication origins. Lack of H3K37me1 results in defective DNA replication from canonical origins while promoting replication events at inefficient and non-canonical sites.

Collectively, our results indicate that H3K37me1 ensures correct execution of the DNA replication program by protecting the genome from inappropriate origin licensing and spurious DNA replication.

 

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Read more about research in the Kouzarides lab.

Watch Tony Kouzarides describe his research on YouTube.

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