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Sex-dependent and -independent X-chromosome histone modifications in Drosophila melanogaster

ABSTRACT: Drosophila X chromosomes are subject to dosage compensation in males and are known to have a specialized chromatin structure in the male soma. We are interested in how specific chromatin structure change contributes to X chromosome hyperactivity and dosage compensation. We have conducted a global analysis of localize two dosage compensation complex dependent histone marks H4AcK16 and H3PS10 and one dosage compensation complex independent histone mark H3diMeK4 in the genome, especially on X chromosome by ChIP-chip approach in both male and female adult flies. We also probed general genomewide chromatin structure by deep DNA sequencing of sheared ChIP input DNA from male and female adult flies.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE15593 | GEO | 2010/01/11

SECONDARY ACCESSION(S): PRJNA115603

REPOSITORIES: GEO

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Sex-dependent and -independent X-chromosome histone modifications in Drosophila melanogaster

Project description:Drosophila X chromosomes are subject to dosage compensation in males and are known to have a specialized chromatin structure in the male soma. We are interested in how specific chromatin structure change contributes to X chromosome hyperactivity and dosage compensation. We have conducted a global analysis of localize two dosage compensation complex dependent histone marks H4AcK16 and H3PS10 and one dosage compensation complex independent histone mark H3diMeK4 in the genome, especially on X chromosome by ChIP-chip approach in both male and female adult flies. We also probed general genomewide chromatin structure by deep DNA sequencing of sheared ChIP input DNA from male and female adult flies. Chromatin immunoprecipitations were performed in 5-7 day aged adult male and female flies with three histone modification antibodies. ChIP enriched DNA and input DNA was labeled by Cy3 or Cy5 dye separately and hybridized simultaneously to the Drosophila FlyGEM arrays. At least two biological replicates were performed for each antibody and sex. DNA-seq (NIDDK-Drosophila-Illumina-DNASeq) were performed on ChIP-input sheared DNA to check the general chromatin structure of different chromosome.

2010-01-11 | E-GEOD-15593 | biostudies-arrayexpress

The activation potential of MOF is constrained for dosage compensation

Project description:The H4K16 acetyltransferase MOF plays a crucial role in dosage compensation in Drosophila, but has additional, global functions. We compared the molecular context and effect of MOF in male and female flies combining chromosome-wide mapping and transcriptome studies with analyses of defined reporter loci in transgenic flies. MOF distributes dynamically between two complexes, the Dosage Compensation Complex and a complex containing MBD-R2, a global facilitator of transcription. These different targeting principles define the distribution of MOF between the X chromosome and autosomes and at transcription units with 5’ or 3’ enrichment. The male X chromosome differs from all other chromosomes in that H4K16 acetylation levels do not correlate with transcription output. The reconstitution of this phenomenon at a model locus revealed that the activation potential of MOF is constraint in male cells in the context of the DCC to arrive at the two-fold activation of transcription characteristic of dosage compensation. ChIP-chip profiling of MBD-R2, MOF and MSL1 in adult male and female flies, and SL2 cells, incl. at least 3 biological replicates

2010-06-26 | E-GEOD-20695 | biostudies-arrayexpress

The activation potential of MOF is constrained for dosage compensation, MBD-R2 transcriptome analysis

Project description:The H4K16 acetyltransferase MOF plays a crucial role in dosage compensation in Drosophila, but has additional, global functions in gene control. We compared the molecular context and effect of MOF activity in male and female flies combining chromosome-wide mapping and transcriptome studies with analyses of defined reporter loci in transgenic flies. MOF distributes dynamically between two types of complexes, the Dosage Compensation Complex (DCC) and complexes containing MBD-R2, a global facilitator of transcription. These different targeting principles define the distribution of MOF between the X chromosome and autosomes and at transcription units with 5’ or 3’ enrichment. The male X chromosome differs from all other chromosomes in that H4K16 acetylation levels do not correlate with transcription output. The reconstitution of this phenomenon at a model locus revealed that the activation potential of MOF is constrained in male cells in the context of the DCC to arrive at the two-fold activation of transcription characteristic of dosage compensation.

2010-06-26 | GSE20744 | GEO

The activation potential of MOF is constrained for dosage compensation

2010-06-26 | GSE20695 | GEO

Sex-biased gene expression in 18 day embryonic chicken heart, brain, and gonad

Project description:The contrasting dose of sex chromosomes in males and females potentially introduces a large-scale imbalance in levels of gene expression between sexes. In many organisms dosage compensation has thus evolved to equalize sex-linked gene expression in males and females1,2, in mammals achieved by X chromosome inactivation and in flies and worms by up- or down-regulation of X-linked expression, respectively. Another form of dosage compensation ensures that expression levels on the X chromosome and on autosomes are balanced3,4. While otherwise widespread in systems with heteromorphic sex chromosomes, the case of dosage compensation in birds (males ZZ, females ZW) remains an unsolved enigma5,6. Here we use a microarray approach to show that male day 18 chicken embryos generally express higher levels of Z-linked genes than female birds, both in soma and in gonads. The distribution of male-to-female fold-change values for Z chromosome genes is wide and has a mean of 1.4-1.6, which is consistent with absence of dosage compensation and sex-specific feedback regulation of gene expression at individual loci2. Intriguingly, without global dosage compensation, female chicken has significantly lower expression levels of Z-linked compared to autosomal genes, which is not the case in male birds. The pronounced sex difference in gene expression is likely to contribute to sexual dimorphism among birds, and potentially has implication to avian sex determination. Keywords: dosage compensation, sex-biased gene expression, soma and gonad

2007-08-07 | GSE8693 | GEO

Histone H4K16 acetylation modulates the dynamics of linker H1 and heterochromatin protein HP1 in male X chromosome dosage compensation

Project description:Drosophila dosage compensation is an epigenetic phenomenon in which the transcription of most genes on X-chromosome is enhanced by approximately two folds in males to equalize that in females. In this study, we provide evidence that transcriptional repressors, such as HP1 and linker histone H1, are globally reduced on male X chromosome. We further investigated the role of HP1 and linker H1 on X chromosome dosage compensation using flies with overexpression of HP1 and H1, we demonstrate that these repressors surpress H4K16 acetylation, presence of the elongating RNA Pol II and the transcription of the genes on male X chromosomes. To understand how H1 and HP1 are regulated on male X chromosome, we next explored the relationship between MOF and the two repressors of chromatin. We show that the hyperacetylation of H4K16 induced by MOF resulted in the loss of H1 and HP1 on chromatin and global chromatin decondensation. Our biochemical analysis further shows that the presence of acetylation on histone H4 at lysine 16 directly inhibits the interaction between histone H4 and linker H1. This study therefore provides novel clues on understanding the dynamic regulation of chromatin regulators on male X chromosome dosage compensation.

2017-11-01 | GSE29537 | 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

The Drosophila Dosage Compensation Complex activates target genes via chromosome looping within the active compartment

Project description:X chromosome dosage compensation in Drosophila requires chromosome-wide coordination of gene activation. The male-specific-lethal dosage compensation complex (DCC) identifies X chromosomal High Affinity Sites (HAS) from which it reaches out to boost transcription. A recently discovered sub-class of HAS, PionX sites, represent first contacts on the X. We explored the chromosomal interactions of representative PionX sites by high-resolution 4C methodology and determined the overall chromosome conformation by Hi-C in sex-sorted embryos. X chromosomes from male and female cells display similar nuclear architecture, concordant with clustered, constitutively active genes. PionX sites, like HAS, are evenly distributed in the active compartment and engage in short- and long-range interactions beyond compartment boundaries. De novo induction of DCC in female cells allowed monitoring the reach of activation surrounding PionX sites. Remarkably, DCC not only activates genes in linear proximity, but also at megabase distance if close in space, suggesting that dosage compensation profits from chromosome folding.

2017-07-01 | GSE94115 | GEO

Synergistic interactions between CLAMP and MSL complex facilitate Drosophila dosage compensation

Project description:ChIP-seq and mRNA-seq experiments were performed to understand the role of the CLAMP protein in dosage compensation ChIP-seq experiments compared the binding profiles of CLAMP in male and female cells and mRNA-seq data to define the role of CLAMP in regulating genes on the X-chromosome

2013-07-15 | E-GEOD-39271 | biostudies-arrayexpress

X Chromosome Dosage Modulates Multiple Molecular and Cellular Properties of Mouse Pluripotent Stem Cells Independently of Global DNA Methylation Levels

Project description:During early mammalian development, the two X-chromosomes in female cells are active. Dosage compensation between XX female and XY male cells is then achieved by X-chromosome inactivation in female cells. Reprogramming female mouse somatic cells into induced pluripotent stem cells (iPSCs) leads to X-chromosome reactivation. The extent to which increased X-chromosome dosage (X-dosage) in female iPSCs leads to differences in the molecular and cellular properties of XX and XY iPSCs is still unclear. We show that chromatin accessibility in mouse iPSCs is modulated by X-dosage. Specific sets of transcriptional regulator motifs are enriched in chromatin with increased accessibility in XX or XY iPSCs. We show that the transcriptome, growth and pluripotency exit are also modulated by X-dosage in iPSCs. To understand the mechanisms by which increased X-dosage modulates the molecular and cellular properties of mouse pluripotent stem cells, we used heterozygous deletions of the X-linked gene Dusp9 in XX embryonic stem cells. We show that X-dosage regulates the transcriptome, open chromatin landscape, growth and pluripotency exit largely independently of global DNA methylation. Our results uncover new insights into X-dosage in pluripotent stem cells, providing principles of how gene dosage modulates the epigenetic and genetic mechanisms regulating cell identity.

2018-03-31 | GSE110215 | GEO

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