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In this study, we found that reduction in H3K27me2\/3 caused by H3.1K27M, a mutation of H3 variants found in patients with diffuse intrinsic pontine glioma (DIPG), dramatically attenuated the presence of 53BP1 (also known as TP53BP1) foci and the capability of non-homologous end joining (NHEJ) in human dermal fibroblasts. H3.1K27M mutant cells showed increased rates of genomic insertions\/deletions and copy number variations, as well as an increase in p53-dependent apoptosis. We further showed that both hypo-H3K27me2\/3 and H3.1K27M interacted with FANCD2, a central player in the choice of DNA repair pathway. H3.1K27M triggered the accumulation of FANCD2 on chromatin, suggesting an interaction between H3.1K27M and FANCD2. Interestingly, knockdown of FANCD2 in H3.1K27M cells recovered the number of 53BP1-positive foci, NHEJ efficiency and apoptosis rate. Although these findings in HDF cells may differ from the endogenous regulation of the H3.1K27M mutant in the specific tumor context of DIPG, our results suggest a new model by which H3K27me2\/3 facilitates NHEJ and the maintenance of genome stability.<\/jats:p>\n               <jats:p>This article has an associated First Person interview with the first author of the paper.<\/jats:p>","DOI":"10.1242\/jcs.215525","type":"journal-article","created":{"date-parts":[[2018,5,14]],"date-time":"2018-05-14T15:55:17Z","timestamp":1526313317000},"source":"Crossref","is-referenced-by-count":43,"title":["Histone H3K27 methylation modulates the dynamics of FANCD2 on chromatin to facilitate NHEJ and genome stability"],"prefix":"10.1242","volume":"131","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9746-6426","authenticated-orcid":false,"given":"Ye","family":"Zhang","sequence":"first","affiliation":[{"name":"School of Medicine, Tsinghua University 1 , Beijing 100084, PR \u2008 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