Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE75855
PROVIDER: PRJNA305540 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2984030.fastq.gz | Fastqsanger.gz | |||
| SRR2984030_1.fastq.gz | Fastqsanger.gz | |||
| SRR2984030_2.fastq.gz | Fastqsanger.gz | |||
| SRR2984023.fastq.gz | Fastqsanger.gz | |||
| SRR2984023_1.fastq.gz | Fastqsanger.gz |
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Project description:High-throughput sequencing of numerous patient samples has identified a myriad of frequent mutations of epigenetic regulators in human cancers, including recently discovered mutations in histone-encoding genes. Lysine-to-methionine mutations such as H3K27M and H3K36M share a common mechanism of inhibiting methylation pathways at the genome-wide level to promote tumorigenesis. However, the mechanism underlying the molecular and cellular changes due to H3G34 alterations is yet to be determined. H3G34 itself is not post-translationally modified; however, G34 lies in close proximity to K36, which undergoes methylation during transcriptional elongation. In Hela cells, H3.3G34L/W mutations have no effect on global levels of methylation on H3K36, H3K27, or other major methylation sites on endogenous histone H3, which include both H3.3 and the canonical H3.1/H3.2 proteins. However, long exposures of the blots revealed that methylation on the ectopic Flag-H3.3 proteins are affected by G34 mutations: with di- and trimethylation on H3K36 and H3K27ac reduced whereas H3K27me3 increased in the G34L and G34W mutated H3.3 compared to the WT H3.3. ChIP-seq results showed that mutations of H3.3G34 affect methylation on H3K36 and H3K27 in cis. G34L/W mutants abolish SETD2 methylation of H3K36. In contrast, the enzymatic activities of both EZH2 and p300 on H3K27 are not affected by G34 mutations. Consistent with changes in H3K27me3 and H3K36m3 levels, we found increased binding of PRC2 (EZH2, SUZ12 and EED) and PRC1 complex components (CBX8 and RING2) and reduced binding of H3.3K36me3 reader such as ZMYND11 to the G34 mutants. In summary, our study revealed that histone H3.3 G34 mutations alter histone K36 and K27 methylation in cis, and affect the binding of readers specific to K36 or K27 methylation.
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Project description:Germ cells have evolved unique mechanisms to ensure an everlasting transmission of their genetic and epigenetic information to future generations, whose alteration compromises germ cell immortality. In many instances, epigenetic factors play fundamental roles in these mechanisms. Despite H3K36 and H3K27 methyltransferases shape and propagate over generations a pattern of histone methylation essential for C. elegans germ cell maintenance, the role of respective histone demethylases in this context remains mainly unexplored. Here, we show that jmjd-5 regulates the level of H3K36me2 and H3K27me3, preserves germ cell immortality at high temperature and protects germ cell identity by controlling somatic and germline gene expression. Strikingly, the biological and transcriptional effects of jmjd-5 loss can be hindered by the removal of demethylases for H3K27, indicating that H3K36/K27 demethylases act in a transcriptional framework and promote the accurate balance between H3K36 and H3K27 methylation required for the maintenance of germ cell immortality. Furthermore, we found that in wild-type, but not in jmjd-5 mutant animals, alterations of H3K27 and H3K36 methylation and transcription occur at high temperature, suggesting a role for jmjd-5 in adaptation to environmental changes.
2021-11-23 | GSE174652 | GEO
Project description:We investigate the contribution of each SUZ12 isoform on PRC2 activity on chromatin using our different ESC lines. As an additional comparison for ∆ex4 cells (SUZ12-S), we included an ESC clone in which an unsuccessful CRISPR editing event resulted in a mutant allele with nearly constitutive splicing of exon 4 (herein, CSex4) and normal Suz12 expression levels (expressing only SUZ12-L). First, we profiled H3K27 bulk PTMs by WB and observed that, while CSex4 cells showed no major differences to control cells, ∆ex4 cells displayed lower levels of H3K27me2 and -me3, with higher levels of mono-methylation and acetylation. Similar results were obtained when comparing SUZ12-L and SUZ12-S ESC rescue lines. To validate these findings with an antibody-independent technique, and to additionally profile other histone PTMs, we analysed these cells with histone-MS. In line with the previous estimates26, WT cells displayed approximately 85% of H3K27 methylation. This proportion was largely similar in CSex4 cells, while it dropped to ~50% in ∆ex4 cells, with H3K27me2 and -me3 being the most affected modifications. Notably, H3K27me2/3 loss in ∆ex4 cells occurred at histone peptides regardless of their H3K36 methylation status. Moreover, the global H3K36 methylation rates were not affected in either CSex4 or ∆ex4 cells (Figure S4C), and no major changes in methylation or acetylation levels were observed at other residues. Importantly, reintroduction of SUZ12-L in KO cells rescued a higher degree of methylation compared to SUZ12-S. Overall, these results indicate that SUZ12-S alone is unable to maintain global physiological levels of H3K27 methylation; rather SUZ12-L is also necessary for this task.
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