Journal
CELL REPORTS
Volume 37, Issue 8, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2021.110050
Keywords
-
Categories
Funding
- NIH Office of Research Infrastructure Programs [P40 OD010440]
- Danish National Research Foundation [DNRF82]
- Italian Association for Cancer Research [IG-2017-20290]
- European Research Council [EC-H2020-ERC-CoG-DissectPcG: 725268]
- FIRC fellowship
Ask authors/readers for more resources
The research found that jmjd-5 regulates H3K36 and H3K27 methylation levels by controlling gene expression, maintaining germ cell immortality and protecting cell identity. H3K36/K27 demethylases play a role in the transcriptional framework, promoting the balance between H3K36 and H3K27 methylation.
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available