Journal
MOLECULAR CELL
Volume 67, Issue 4, Pages 550-+Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2017.07.012
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Funding
- Institut National du Cancer (INCa)
- Fondation Tourre
- RIKEN Junior Research Associate Program
- Association pour la Recherche contre le Cancer (ARC)
- Institut National du Cancer (INCa PLBio)
- Groupement des Entreprises Francaises dans la Lutte contre le Cancer (GEFLUC)
- Agence Nationale de la Recherche [ANR-15-CE12-0012-01, ANR-11-LABX-0071/ANR-11-IDEX-0005-01]
- Dana-Farber Strategic Research Initiative
- NIH [CA042368-30]
- Medical Research Council (MRC)
- European Research Council (ERC-CoG dynamicmodifications'')
- RIKEN
- Deutsche Forschungsgemeinschaft (DFG) [SFB1064/A17]
- MRC [MC_U120092689] Funding Source: UKRI
- Medical Research Council [MC_U120092689] Funding Source: researchfish
- Grants-in-Aid for Scientific Research [26250039] Funding Source: KAKEN
- Agence Nationale de la Recherche (ANR) [ANR-15-CE12-0012] Funding Source: Agence Nationale de la Recherche (ANR)
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DNA methylation is an essential epigenetic mark in mammals that has to be re-established after each round of DNA replication. The protein UHRF1 is essential for this process; it has been proposed that the protein targets newly replicated DNA by cooperatively binding hemi-methylated DNA and H3K9me2/3, but this model leaves a number of questions unanswered. Here, we present evidence for a direct recruitment of UHRF1 by the replication machinery via DNA ligase 1 (LIG1). A histone H3K9-like mimic within LIG1 is methylated by G9a and GLP and, compared with H3K9me2/3, more avidly binds UHRF1. Interaction with methylated LIG1 promotes the recruitment of UHRF1 to DNA replication sites and is required for DNA methylation maintenance. These results further elucidate the function of UHRF1, identify a non-histone target of G9a and GLP, and provide an example of a histone mimic that coordinates DNA replication and DNA methylation maintenance.
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