ArticleNucleic acids research2020
HP1γ regulates H3K36 methylation and pluripotency in embryonic stem cells.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 27 citations in OpenAlex.
- BRD4 recruitment into HP1 condensates desilences transcription without erasure of repressive chromatin.Nature cell biology · 2026Article
- Article
- CGRP causes anxiety via HP1γ-KLF11-MAOB pathway and dopamine in the dorsal hippocampus.Communications biology · 2024Article
- KDM3A and KDM3B Maintain Naïve Pluripotency Through the Regulation of Alternative Splicing.bioRxiv : the preprint server for biology · 2024Article
- CBX3 promotes clear cell renal carcinoma through PI3K/AKT activation and aberrant immunity.Journal of translational medicine · 2023Article
- The regulation of transcription elongation in embryonic stem cells.Frontiers in cell and developmental biology · 2023Review
- Age reprogramming: cell rejuvenation by partial reprogramming.Development (Cambridge, England) · 2022Article
- Comprehensive pan-cancer analysis on CBX3 as a prognostic and immunological biomarker.BMC medical genomics · 2022Article
- Article
- H3K36 methylation reprograms gene expression to drive early gametocyte development in Plasmodium falciparum.Epigenetics & chromatin · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The heterochromatin protein 1 (HP1) family members are canonical effectors and propagators of gene repression mediated by histone H3 lysine 9 (H3K9) methylation. HP1γ exhibits an increased interaction with active transcription elongation-associated factors in embryonic stem cells (ESCs) compared to somatic cells. However, whether this association has a functional consequence remains elusive. Here we find that genic HP1γ colocalizes and enhances enrichment of transcription elongation-associated H3K36me3 rather than H3K9me3. Unexpectedly, sustained H3K36me3 deposition is dependent on HP1γ. HP1γ-deleted ESCs display reduced H3K36me3 enrichment, concomitant with decreased expression at shared genes which function to maintain cellular homeostasis. Both the H3K9me3-binding chromodomain and histone binding ability of HP1γ are dispensable for maintaining H3K36me3 levels. Instead, the chromoshadow together with the hinge domain of HP1γ that confer protein and nucleic acid-binding ability are sufficient because they retain the ability to interact with NSD1, an H3K36 methyltransferase. HP1γ-deleted ESCs have a slower self-renewal rate and an impaired ability to differentiate towards cardiac mesoderm. Our findings reveal a requirement for HP1γ in faithful establishment of transcription elongation in ESCs, which regulates pluripotency.
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Registered trials
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