ArticleCell reports2021
Coordinated maintenance of H3K36/K27 methylation by histone demethylases preserves germ cell identity and immortality.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Towards naturalistic social neuroscience: A multi-level framework integrating real-world phenotyping, neurobiology, and computational mechanisms.Cognitive, affective & behavioral neuroscience · 2026Review
- Hypoxia-induced metastatic heterogeneity in pancreatic cancer.Nature communications · 2026Article
- The transcription factor LSL-1 interacts with the chromatin factors HIM-17, XND-1 and BRA-2 to promote the germline-specific transcriptional repertoire and to safeguard germ cell fate inbioRxiv : the preprint server for biology · 2026Article
- Functional dissection of H3K4 methyltransferases reveals distinct catalytic and non-catalytic roles in C. elegans development.Development (Cambridge, England) · 2025Article
- The chromatin remodeler LET-418/Mi-2 regulates the intracellular pathogen response in the C. elegans intestine.BMC genomics · 2025Article
- Hypoxia-induced metastatic heterogeneity in pancreatic cancer.Research square · 2025Article
- Intracellular CaBiologia futura · 2025Review
- Transcriptional co-activators: emerging roles in signaling pathways and potential therapeutic targets for diseases.Signal transduction and targeted therapy · 2023Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Germ cells have evolved unique mechanisms to ensure the transmission of genetically and nongenetically encoded information, whose alteration compromises germ cell immortality. Chromatin factors play fundamental roles in these mechanisms. H3K36 and H3K27 methyltransferases shape and propagate a pattern of histone methylation essential for C. elegans germ cell maintenance, but the role of respective histone demethylases remains unexplored. Here, we show that jmjd-5 regulates H3K36me2 and H3K27me3 levels, preserves germline immortality, and protects germ cell identity by controlling gene expression. The transcriptional and biological effects of jmjd-5 loss can be hindered by the removal of H3K27demethylases, indicating that H3K36/K27 demethylases act in a transcriptional framework and promote the balance between H3K36 and H3K27 methylation required for germ cell immortality. Furthermore, we find that in wild-type, but not in jmjd-5 mutants, alterations of H3K36 methylation and transcription occur at high temperature, suggesting a role for jmjd-5 in adaptation to environmental changes.
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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.