ArticleEpigenetics2017
An HP1 isoform-specific feedback mechanism regulates Suv39h1 activity under stress conditions.
Article in Epigenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- The timing of maternal protein degradation during mammalian preimplantation development is species-specific.Reproduction (Cambridge, England) · 2025Article
- Senescence-associated alterations in histone H3 modifications, HP1 alpha levels and distribution, and in the transcriptome of vascular smooth muscle cells in different types of senescence.Cell communication and signaling : CCS · 2025Article
- Increased H3K9me3 and F-Actin Reorganization in the Rapid Adaptive Response to Hypergravity in Human T Lymphocytes.International journal of molecular sciences · 2023Article
- HP1 proteins regulate nucleolar structure and function by secluding pericentromeric constitutive heterochromatin.Nucleic acids research · 2023Article
- A complex interplay between H2A.Z and HP1 isoforms regulates pericentric heterochromatin.Frontiers in cell and developmental biology · 2023Article
- HP1 maintains protein stability of H3K9 methyltransferases and demethylases.EMBO reports · 2022Article
- Enzymology of Mammalian DNA Methyltransferases.Advances in experimental medicine and biology · 2022Article
- HP1β carries an acidic linker domain and requires H3K9me3 for phase separation.Nucleus (Austin, Tex.) · 2021Article
- Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications.International journal of molecular sciences · 2021Review
- The Histone Code of Senescence.Cells · 2020Review
- Nuclear Organization in Stress and Aging.Cells · 2019Review
- Slowing Down Ageing: The Role of Nutrients and Microbiota in Modulation of the Epigenome.Nutrients · 2019Review
- The Role of Phase Separation in Heterochromatin Formation, Function, and Regulation.Biochemistry · 2018Review
- Deletion of HP1γ in cardiac myocytes affects H4K20me3 levels but does not impact cardiac growth.Epigenetics & chromatin · 2018Article
- Zfp296 negatively regulates H3K9 methylation in embryonic development as a component of heterochromatin.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The presence of H3K9me3 and heterochromatin protein 1 (HP1) are hallmarks of heterochromatin conserved in eukaryotes. The spreading and maintenance of H3K9me3 is effected by the functional interplay between the H3K9me3-specific histone methyltransferase Suv39h1 and HP1. This interplay is complex in mammals because the three HP1 isoforms, HP1α, β, and γ, are thought to play a redundant role in Suv39h1-dependent deposition of H3K9me3 in pericentric heterochromatin (PCH). Here, we demonstrate that despite this redundancy, HP1α and, to a lesser extent, HP1γ have a closer functional link to Suv39h1, compared to HP1β. HP1α and γ preferentially interact in vivo with Suv39h1, regulate its dynamics in heterochromatin, and increase Suv39h1 protein stability through an inhibition of MDM2-dependent Suv39h1-K87 polyubiquitination. The reverse is also observed, where Suv39h1 increases HP1α stability compared HP1β and γ. The interplay between Suv39h1 and HP1 isoforms appears to be relevant under genotoxic stress. Specifically, loss of HP1α and γ isoforms inhibits the upregulation of Suv39h1 and H3K9me3 that is observed under stress conditions. Reciprocally, Suv39h1 deficiency abrogates stress-dependent upregulation of HP1α and γ, and enhances HP1β levels. Our work defines a specific role for HP1 isoforms in regulating Suv39h1 function under stress via a feedback mechanism that likely regulates heterochromatin formation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.