Set2 and H3K36 regulate the Drosophila male X chromosome in a context-specific manner (WL3 brain)
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ABSTRACT:
PROVIDER: PRJNA1128523 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29553136_1.fastq.gz | Fastqsanger.gz | |||
| SRR29553136_2.fastq.gz | Fastqsanger.gz | |||
| SRR29553137_1.fastq.gz | Fastqsanger.gz | |||
| SRR29553137_2.fastq.gz | Fastqsanger.gz | |||
| SRR29553138_1.fastq.gz | Fastqsanger.gz |
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Project description:Current models of MSL spreading in the context of Drosophila dosage compensation (DC) focus on interactions of MSL3 (male-specific lethal 3) with histone marks; especially Set2-dependent H3 lysine-36 trimethylation (H3K36me3). However, previous studies investigating the role of H3K36me3 in DC do not fully account for: other targets of Set2, redundancy between canonical H3.2 and replication-dependent H3.3, and X chromosome effects that are not sex-specific.To differentiate amongst these possibilities and to assess whether Set2 and/or H3K36 is essential for DC, we use RNA-Seq in WL3 brain (male and female) and L1 larvae (mixed sex) to compare Set2, H3.2K36R, H3.3K36R, and combined H3K36R mutant genotypes. In brains, we observe heterogeneous regulation of chrX genes by these factors in both males and females. These effects are not clearly linked to MSL3 binding or H4K16ac occupancy, but in some groups of genes, are clearly stronger in males. At L1, we also observe heterogeneous gene regulation distinct from an H4K16R control. Simultaneous mutation of both H3.2K36 and H3.3K36 results in an increase in expression in genes most strongly reduced in H4K16R mutants. Overall, the data are inconsistent with the prevailing model wherein H3K36me3 is essential for spreading the MSL complex to genes along the male X. Rather, we propose that Set2 and H3K36 support DC indirectly, via processes that are utilized by MSL, but common to both sexes.
2024-10-14 | GSE270800 | GEO
Project description:Current models of MSL spreading in the context of Drosophila dosage compensation (DC) focus on interactions of MSL3 (male-specific lethal 3) with histone marks; especially Set2-dependent H3 lysine-36 trimethylation (H3K36me3). However, previous studies investigating the role of H3K36me3 in DC do not fully account for: other targets of Set2, redundancy between canonical H3.2 and replication-dependent H3.3, and X chromosome effects that are not sex-specific.To differentiate amongst these possibilities and to assess whether Set2 and/or H3K36 is essential for DC, we use RNA-Seq in WL3 brain (male and female) and L1 larvae (mixed sex) to compare Set2, H3.2K36R, H3.3K36R, and combined H3K36R mutant genotypes. In brains, we observe heterogeneous regulation of chrX genes by these factors in both males and females. These effects are not clearly linked to MSL3 binding or H4K16ac occupancy, but in some groups of genes, are clearly stronger in males. At L1, we also observe heterogeneous gene regulation distinct from an H4K16R control. Simultaneous mutation of both H3.2K36 and H3.3K36 results in an increase in expression in genes most strongly reduced in H4K16R mutants. Overall, the data are inconsistent with the prevailing model wherein H3K36me3 is essential for spreading the MSL complex to genes along the male X. Rather, we propose that Set2 and H3K36 support DC indirectly, via processes that are utilized by MSL, but common to both sexes.
2024-10-14 | GSE270799 | GEO
Project description:Set2 and H3K36 regulate the Drosophila male X chromosome in a context-specific manner (L1)
| PRJNA1128524 | ENA
Project description:The transcription elongation factor Spt6 and the H3K36 methyltransferase Set2 are both required for H3K36 methylation and transcriptional fidelity in Saccharomyces cerevisiae. By selecting for suppressors of a transcriptional defect in an spt6 mutant, we have isolated dominant SET2 mutations (SET2sup mutations) in a region encoding a proposed autoinhibitory domain. The SET2sup mutations suppress the H3K36 methylation defect in the spt6 mutant, as well as in other mutants that impair H3K36 methylation. ChIP-seq studies demonstrate that the H3K36 methylation defect in the spt6 mutant, as well as its suppression by a SET2sup mutation, occur at a step following the recruitment of Set2 to chromatin. Other experiments show that a similar genetic relationship between Spt6 and Set2 exists in Schizosaccharomyces pombe. Taken together, our results suggest a conserved mechanism by which the Set2 autoinhibitory domain requires multiple interactions to ensure that H3K36 methylation occurs specifically on actively transcribed chromatin.
2019-02-13 | GSE116646 | GEO
Project description:Histone H3K36 can be added up to three methyl groups to form mono-, di-, and tri-methylation states. Recent study has shown that Set2 can suppress a specific group of antisense transcripts, which largely depends on the presence of H3K36 methylation. However, whether different methylation states possess distinct regulatory mechanisms on antisense transcripts is still unclear. In this study, we identified two yeast mutants that lack H3K36 di-methylation and tri-methylation, respectively. We also identified novel antisense transcripts in the absence of Set2 with own bioinformatics pipeline. Our study showed that the expression of these antisense transcripts does not affect the expression of corresponding sense genes. Different H3K36 methylation states (me2/me3) are not specific for the regulation of antisense expression, implying a co-regulation mechanism between them. Altogether, our study developed a method to identify new antisense transcripts, examined the potential effect of H3K36 di-methylation and tri-methylation on production of antisense transcripts. This study would shed light on the mechanism underlying how H3K36 methylation functions in the production of antisense transcripts.
2021-06-19 | GSE167338 | GEO
Project description:In Drosophila, two chromosomes require special mechanisms to balance their transcriptional output to the rest of the genome. These are the male-specific lethal complex targeting the male X chromosome and Painting of fourth targeting chromosome 4. Here, we explore the role of histone H3 methylated at lysine-36 (H3K36) and the associated methyltransferases—Set2, NSD, and Ash1—in these two chromosome-specific systems. We show that the loss of Set2 impairs the MSL complex–mediated dosage compensation; however, the effect is not recapitulated by H3K36 replacement and indicates an alternative target of Set2. Unexpectedly, balanced transcriptional output from the fourth chromosome requires intact H3K36 and depends on the additive functions of NSD and Ash1. We conclude that H3K36 methylation and the associated methyltransferases are important factors to balance transcriptional output of the male X chromosome and the fourth chromosome. Furthermore, our study highlights the pleiotropic effects of these enzymes.
2021-08-10 | GSE166934 | GEO
Project description:H3K36 methylation by Set2 targets Rpd3S histone deacetylase to 3â transcribed regions, repressing internal cryptic promoters and slowing elongation. To further explore the function of this pathway, global transcription was analyzed in yeast experiencing a series of carbon source shifts. Many previously unreported cryptic ncRNAs are induced by specific carbon sources, showing that cryptic promoters can be environmentally regulated. Also, approximately 230 mRNA genes show altered induction or repression upon SET2 deletion. A majority of Set2-repressed genes have overlapping lncRNA transcription. At these promoters, H3K36me3 and deacetylation by Rpd3S leads to slower or reduced induction. Unexpectedly, Set2 derepresses 159 genes, apparently by mediating a balance between Rpd3S and Rpd3L. Therefore, in addition to repression of cryptic transcription, H3K36 methylation maintains optimal expression dynamics of many mRNAs.
2016-09-25 | E-MTAB-4268 | biostudies-arrayexpress
Project description:Histone H3 lysine 36 methylation (H3K36me) is a conserved histone modification associated with transcription and DNA repair. Although the effects of H3K36 methylation have been studied, the genome-wide dynamics of H3K36me deposition and removal are not known. We established rapid and reversible optogenetic control for Set2, the sole H3K36 methyltransferase in yeast, by fusing the enzyme with the light activated nuclear shuttle (LANS) domain. Early H3K36me3 dynamics identified methylation in vivo, with total H3K36me3 levels correlating with RNA abundance. Although genes exhibited disparate levels of H3K36 methylation, relative rates of H3K36me3 accumulation were largely linear and consistent across genes, suggesting that H3K36me3 deposition occurs uniformly across all genes in a directed fashion regardless of transcription frequency. Removal of H3K36me3 was highly dependent on the demethylase Rph1. However, the per-gene rate of H3K36me3 loss weakly correlated with RNA abundance and followed exponential decay, suggesting H3K36 demethylases act in a global, stochastic manner. Altogether, these data provide a detailed temporal view of H3K36 methylation and demethylation that suggest transcription-dependent and independent mechanisms for H3K36me deposition and removal, respectively.
2020-07-01 | GSE153539 | GEO
Project description:In budding yeast, Set2 catalyzes di- and trimethylation of H3K36 (H3K36me2 and H3K36me3) via an interaction between its SRI domain and C-terminal repeats of RNA polymerase II (Pol2) phosphorylated at Ser2 and Ser5 (CTD-S2,5-P). H3K36me2 recruits the Rpd3S histone deacetylase complex to repress cryptic transcription from transcribed regions. In fission yeast, Set2 is also responsible for H3K36 methylation, which represses a subset of RNAs including heterochromatic and subtelomeric RNAs, at least in part via recruitment of Clr6 complex II, a homolog of Rpd3S. Here, we show that CTD-S2Pâdependent interaction of fission yeast Set2 with Pol2 via the SRI domain is required for formation of H3K36me3, but not H3K36me2. H3K36me3 silenced heterochromatic and subtelomeric transcripts through post-transcriptional and transcriptional mechanisms, respectively, whereas H3K36me2 did not. Clr6 complex II appeared not to be responsible for heterochromatic silencing. Our results demonstrate that H3K36 methylation has multiple outputs in fission yeast; these findings provide insight into the multiple roles of H3K36 methylation in metazoans, which have different enzymes for synthesis of H3K36me1/2 and H3K36me3. Gene expression profile at exponentially-growing phase.in the fission yeast deletion mutants of set2.
2016-02-04 | E-GEOD-66821 | biostudies-arrayexpress
Project description:We characterized the role of H3K36 methylation in regulating repair of UV damage from the transcribed strand (TS) of yeast genes by the transcription coupled nucleotide excision repair (TC-NER) pathway. TC-NER is triggered when RNA polymerase stalls at UV damage, such as a UV-induced cyclobutane pyrimidine dimer (CPD). During transcription, the histone methyltransferase Set2 methylates histone H3K36, but it is not known if H3K36 methylation regulates TC-NER. Here, we report genome-wide repair maps of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast cells containing mutants in histone H3K36 (or set2).
2022-02-21 | GSE194101 | GEO