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Set2 and H3K36 regulate the Drosophila male X chromosome in a context-specific manner (WL3 brain)

ABSTRACT: Set2 and H3K36 regulate the Drosophila male X chromosome in a context-specific manner (WL3 brain)

PROVIDER: PRJNA1128523 | ENA |

REPOSITORIES: ENA

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			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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Similar Datasets

Set2 and H3K36 regulate the Drosophila male X chromosome in a context-specific manner (L1)

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

Set2 and H3K36 regulate the Drosophila male X chromosome in a context-specific manner (WL3 brain)

2024-10-14 | GSE270799 | GEO

Set2 and H3K36 regulate the Drosophila male X chromosome in a context-specific manner (L1)

Project description:Set2 and H3K36 regulate the Drosophila male X chromosome in a context-specific manner (L1)

| PRJNA1128524 | ENA

A conserved genetic interaction between Spt6 and Set2 regulates H3K36 methylation

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

Set2 and H3K36 regulate the Drosophila male X chromosome in a context-specific manner, independent from MSL complex spreading.

Project description: Not available

| S-EPMC11631440 | biostudies-literature

Set2 and H3K36 regulate the <i>Drosophila</i> male X chromosome in a context-specific manner, independent from MSL complex spreading.

Project description: Not available

| S-EPMC11100620 | biostudies-literature

Regulation of the histone H3K36 methyltransferase Set2 by the histone chaperone Spt6 [ChIP-Seq]

Project description:Histone H3 lysine 36 methylation is a conserved histone modification that is critical for maintaining eukaryotic transcriptional fidelity and genomic stability. In Saccharomyces cerevisiae, this modification is catalyzed by Set2, an ortholog of the mammalian H3K36 methyltransferase SETD2. Previous genetic, biochemical, and structural studies showed that Set2 activity is repressed by a Set2 autoinhibitory domain (AID) and that activation requires the direct binding of the histone chaperone Spt6. To study the role of Spt6 and Set2 autoinhibition in vivo, we have isolated and analyzed multiple classes of Spt6 and Set2 mutants. Our results suggest an autoinhibited form of Set2 in which the catalytic domain is bound by the AID. In strong agreement with our genetic results, biophysical experiments demonstrate that the catalytic domain and AID physically interact, and that the autoinhibition mutants disrupt this interaction. Finally, RNA-seq and ChIP-seq studies show the importance of the Set2-Spt6 interaction for transcription and H3K36 methylation genome-wide. Taken together, our results support a model in which Set2 exists in an inactive, autoinhibited state in vivo through direct catalytic domain-AID interactions, with binding by Spt6 required to relieve this autoinhibited state.

2026-05-20 | GSE332555 | GEO

Regulation of the histone H3K36 methyltransferase Set2 by the histone chaperone Spt6 [RNA-seq]

2026-05-20 | GSE331502 | GEO

Set2-mediated H3K36 methylation states redundantly repress the production of antisense transcripts:: role in transcription regulation

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

The role of H3K36 methylation and associated methyl transferases in chromosome-specific gene regulation

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

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