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MSL complex is attracted to genes marked by H3K36 trimethylation using a sequence-independent mechanism

ABSTRACT: In Drosophila, X chromosome dosage compensation requires the male-specific lethal (MSL) complex, which associates with actively transcribed genes on the single male X chromosome to upregulate transcription approximately 2-fold. We found that on the male X chromosome, or when MSL complex is ectopically localized to an autosome, histone H3K36 trimethylation (H3K36me3) is a strong predictor of MSL binding. We isolated mutants lacking Set2, the H3K36me3 methyltransferase, and found that Set2 is an essential gene in both sexes of Drosophila. In set2 mutant males, MSL complex maintains X specificity but exhibits reduced binding to target genes. Furthermore, recombinant MSL3 protein preferentially binds nucleosomes marked by H3K36me3 in vitro. Our results support a model in which MSL complex uses high-affinity sites to initially recognize the X chromosome and then associates with many of its targets through sequence-independent features of transcribed genes. Keywords: ChIP-chip

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE8557 | GEO | 2007/09/20

SECONDARY ACCESSION(S): PRJNA101701

REPOSITORIES: GEO

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MSL complex is attracted to genes marked by H3K36 trimethylation using a sequence-independent mechanism

Project description:In Drosophila, X chromosome dosage compensation requires the male-specific lethal (MSL) complex, which associates with actively transcribed genes on the single male X chromosome to upregulate transcription approximately 2-fold. We found that on the male X chromosome, or when MSL complex is ectopically localized to an autosome, histone H3K36 trimethylation (H3K36me3) is a strong predictor of MSL binding. We isolated mutants lacking Set2, the H3K36me3 methyltransferase, and found that Set2 is an essential gene in both sexes of Drosophila. In set2 mutant males, MSL complex maintains X specificity but exhibits reduced binding to target genes. Furthermore, recombinant MSL3 protein preferentially binds nucleosomes marked by H3K36me3 in vitro. Our results support a model in which MSL complex uses high-affinity sites to initially recognize the X chromosome and then associates with many of its targets through sequence-independent features of transcribed genes. Keywords: ChIP-chip ChIP-chip experiments were performed on custom Nimblegen arrays (GPL5636). Each array contained 388,000 oligonucleotide probes covering all of the X and the 2L chromosomes, with a 100 bp resolution (50mer probes with 50 bp gaps). The design was based on FlyBase 3.2. For the superspreading experiments, an additional array was used that contains the entire X chromosome and 3R (GPL5660). MSL complex binding sites on both arrays are the same and signal on the 3R chromosome was at background level.

2007-09-20 | E-GEOD-8557 | biostudies-arrayexpress

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

Drosophila MSL complex globally acetylates H4 Lys16 on the male X chromosome for dosage compensation

2009-06-10 | GSE14884 | GEO

MSL3 coordinates a transcriptional and translational meiotic program in female Drosophila

Project description:Gamete formation from germline stem cells (GSCs) is essential for sexual reproduction. However, the regulation of GSC differentiation and meiotic entry are incompletely understood. Set2, which deposits H3K36me3 modifications, is required for differentiation of GSCs during Drosophila oogenesis. We discovered that the H3K36me3 reader Male-specific lethal 3 (MSL3) and the histone acetyltransferase complex Ada2a-containing (ATAC) cooperate with Set2 to regulate entry into meiosis in female Drosophila. MSL3 expression is restricted to the mitotic and early meiotic stages of the female germline, where it promotes transcription of genes encoding synaptonemal complex components and a germline enriched ribosomal protein S19 paralog, RpS19b. RpS19b upregulation is required for translation of Rbfox1, a known meiotic cell cycle entry factor. Thus, MSL3 is a master regulator of meiosis, coordinating the expression of factors required for recombination and GSC differentiation. We find that MSL3 is expressed during mouse spermatogenesis, suggesting a conserved function during meiosis.

2021-12-09 | GSE143728 | GEO

Sequence variation within similar cis-elements promotes context-specific functions of two Drosophila GA-binding transcription factors (ChIP-seq data set)

Project description:A key model for understanding how large transcription complexes are targeted is the Drosophila dosage compensation system in which the Male-Specific Lethal (MSL) transcription complex specifically identifies and regulates the male X-chromosome. MSL complex is targeted to GA-containing sequences, but the most well-studied GA-binding transcription factor, GAGA Associated Factor (GAF), does not physically associate with MSL complex. Instead the Chromatin Linked Adapter for MSL Proteins (CLAMP) zinc-finger protein specifically targets MSL complex to GA-rich sequences on the X-chromosome. Here, we compare the binding relationships of CLAMP, GAF, and the MSL3 dosage compensation complex protein using ChIP-seq.

2018-02-01 | GSE107059 | GEO

Non-coding roX RNAs Prevent the Binding of the MSL-complex to Heterochromatic Regions

Project description:Long non-coding RNAs are involved in dosage compensation both in mammals and in Drosophila by inducing changes in the X-chromosome chromatin structure. In Drosophila melanogaster, roX1 and roX2 are long non-coding RNAs that together with proteins form the male-specific lethal (MSL) complex, which coats the entire male X-chromosome and mediates dosage compensation by increased transcriptional output. It has been shown that in polytene chromosomes, in absence of both roX1 and roX2, the MSL-complex is decreased on the male X-chromosome and found relocated to the chromocenter, and the 4th chromosome. Here we address the role of roX RNAs in MSL-complex targeting and in the evolution of dosage compensation in Drosophila. We performed ChIP-seq experiments and show that MSL-complex recruitment to high affinity sites (HAS) on the X-chromosome is independent on roX and that the HAS sequence motif is conserved in D. simulans. Additionally, a complete and enzymatically active MSL-complex is recruited to six specific genes on the 4th chromosome. Interestingly, our sequence analysis shows that in the absence of roX RNAs, the MSL-complex has affinity to regions enriched in Hoppel transposable elements and to repeats in general. We hypothesize that roX mutants reveal an ancient targeting of the MSL-complex and propose that the role of roX RNAs is to restrict MSL-complex from binding to heterochromatin.

2014-11-07 | GSE58768 | GEO

Drosophila MSL complex selectively identifies active genes on the male X chromosome

Project description:X-chromosome dosage compensation in Drosophila requires the male-specific lethal (MSL) complex, which up-regulates gene expression from the single male X chromosome. Here, we define X-chromosome-specific MSL binding at high resolution in two male cell lines and in late-stage embryos. We find that the MSL complex is highly enriched over most expressed genes, with binding biased toward the 3' end of transcription units. The binding patterns are largely similar in the distinct cell types, with ~600 genes clearly bound in all three cases. Genes identified as clearly bound in one cell type and not in another indicate that attraction of MSL complex correlates with expression state. Thus, sequence alone is not sufficient to explain MSL targeting. We propose that the MSL complex recognizes most X-linked genes, but only in the context of chromatin factors or modifications indicative of active transcription. Distinguishing expressed genes from the bulk of the genome is likely to be an important function common to many chromatin organizing and modifying activities. Keywords: ChIP-chip

2007-08-01 | GSE8575 | GEO

Drosophila MSL complex globally acetylates H4 Lys16 on the male X chromosome for dosage compensation

Project description:Drosophila MSL complex binds the single male X chromosome to upregulate gene expression to equal that from the two female X chromosomes. However, it has been puzzling that ~25% of transcribed genes on the X do not stably recruit MSL complex. Here, we find that almost all active genes on the X are associated with robust H4 Lys16 acetylation (H4K16ac), the histone modification catalyzed by MSL complex. The distribution of H4K16ac is much broader than that of MSL complex, and our results favor the idea that chromosome-wide H4K16ac reflects transient association of MSL complex, occurring through spreading or chromosomal looping. Our results parallel those of localized Polycomb repressive complex and its more broadly distributed H3K27me3 chromatin mark, suggesting a common principle for the establishment of active and silenced chromatin domains For ChIP-on-chip experiments in larvae, 1000 third instar larvae were collected and chromatin was prepared as described previously. Five IPs were performed for each of the two biological replicates. For SL2 cells and male larvae, one ChIP-on-chip experiment was performed using anti-H4K16ac from Serotec (AHP417) (1-2 ul/IP). However, this antibody was discontinued, and an additional experiment for each was performed using anti-H4K16ac from Upstate/Millipore (07-329) (3 ul/IP). Both replicates for Kc cells and female larvae were also performed using anti-H4K16ac from Upstate/Millipore. Replicate experiments were highly reproducible.

2009-06-10 | E-GEOD-14884 | biostudies-arrayexpress

Long range spreading of dosage compensation in Drosophila captures transcribed autosomal genes inserted on X

Project description:Dosage compensation in D. melanogaster males is achieved via targeting of the MSL complex to X chromosomal genes. This is proposed to involve initial sequence-specific recognition of the X at ~150-300 chromatin entry sites, and subsequent spreading to nearby active genes. Here we test a model in which the spreading step requires transcription and is sequence-independent. We ask whether, in the native context of the X chromosome, MSL complex will target genes of autosomal origin. We find that MSL complex does bind such genes, but only if transcriptionally active. Targeting is accompanied by acetylation of the histone H4K16 residue and two-fold transcriptional up-regulation. We conclude that the presence of a long-sought specific DNA sequence within X-linked genes is not obligatory for MSL complex binding. Instead, physical linkage and transcription play the pivotal roles in the identification of MSL targets irrespective of their origin and DNA sequence. Keywords: Epigenetics ChIP-seq measurements of MSL complex binding and input control. Chromatin was prepared from third instar male larvae of a genotype y w TrojanElephant; MSL3-TAP; msl3. TrojanElephant is a mini-white- and yellow-marked transposition of genomic region spanning 65 kb from cg13773 to snRNP70K. MSL3-TAP is a mini-white-marked TAP-tagged genomic msl3 transgene. IgG beads were used for pull-down.

2009-08-20 | E-GEOD-17729 | biostudies-arrayexpress

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