ArticleNature communications2026
Mammalian DNA maintenance methylation depends on histone but not PAF15 ubiquitination.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
In mammals, DNA methylation is an essential inheritable epigenetic modification maintained by the DNMT1-UHRF1 machinery in a UHRF1 E3 ubiquitin ligase-activity-dependent manner. UHRF1-catalyzed histone ubiquitination and PAF15 ubiquitination have been proposed to recruit DNMT1 to hemi-methylated CpGs. Here, we confirm that both PAF15 and histone H3 are robustly ubiquitinated by UHRF1 in a replication-dependent manner during S phase. However, loss of PAF15 or its ubiquitination, or overexpression of ubiquitination-deficient PAF15, does not alter DNMT1 recruitment to replicating DNA or global DNA methylation. Notably, the DNMT1 inhibitor GSK-3685032 strongly enhances histone ubiquitination, likely via UHRF1 activation driven by accumulated hemi-methylated CpGs, but markedly reduces PAF15 ubiquitination. We show that UHRF1-mediated PAF15 ubiquitination requires DNMT1, is strictly replication-coupled, and that PAF15 and histone ubiquitination are mediated by distinct UHRF1 pools. Taken together, our study demonstrates that hemi-methylated-DNA-stimulated local histone ubiquitination, rather than replication-coupled PAF15 ubiquitination, drives DNMT1 targeting for maintenance methylation.
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