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Caenorhabditis elegans

ABSTRACT: An H4K16 histone acetyltransferase mediates decondensation of the X chromosome in C. elegans males

PROVIDER: PRJNA328790 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3879840.fastq.gz	Fastqsanger.gz
	SRR3879850.fastq.gz	Fastqsanger.gz
	SRR3879860.fastq.gz	Fastqsanger.gz
	SRR3879870.fastq.gz	Fastqsanger.gz
	SRR3879880.fastq.gz	Fastqsanger.gz

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An H4K16 histone acetyltransferase mediates decondensation of the X chromosome in C. elegans males

Project description:In C. elegans, in order to equalize gene expression between the sexes and balance X and autosomal expression, two steps are believed to be required. First, an unknown mechanism is hypothesized to upregulate the X chromosome in both sexes. This mechanism balances the X to autosomal expression in males, but creates X overexpression in hermaphrodites. Therefore, to restore the balance, hermaphrodites downregulate gene expression twofold on both X chromosomes. While many studies have focused on X chromosome downregulation, the mechanism of X upregulation is not known. To gain more insight into X upregulation, we studied the effects of chromatin condensation and histone acetylation on gene expression levels in male C. elegans. We have found that the H4K16 histone acetyltransferase MYS-1/Tip60 mediates dramatic decondensation of the male X chromosome as measured by FISH. However, RNA-seq analysis revealed that MYS-1 contributes only slightly to upregulation of gene expression on the X chromosome. These results suggest that the level of chromosome decondensation does not necessarily correlate with the degree of gene expression change in vivo. Furthermore, the X chromosome is more sensitive to MYS-1-mediated decondensation than the autosomes, despite similar levels of H4K16ac on all chromosomes, as measured by ChIP-seq. H4K16ac levels weakly correlate with gene expression levels on both the X and the autosomes, but highly expressed genes on the X chromosome do not contain exceptionally high levels of H4K16ac.These results indicate that H4K16ac and chromosome decondensation influence regulation of the male X chromosome; however, they do not fully account for the high levels of gene expression observed on the X chromosomes.

2016-10-12 | GSE84307 | 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.

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Project description:Histone marks in C. elegans IKB mutants

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Cooperation between Caenorhabditis elegans COMPASS and condensin in germline chromatin organization

Project description:Deposition of histone H3 lysine 4 (H3K4) methylation at promoter regions by the SET1/COMPASS complex is associated with context-dependent effects on gene expression. Transcription-independent functions have also been attributed to this highly conserved complex, but whether these contribute to higher-order chromosome organization has not been explored. Using a quantitative FRET (Förster resonance energy transfer)-based fluorescence lifetime imaging microscopy (FLIM) approach to assay nanometer scale chromatin compaction in live animals, we reveal an unexpected role for SET1/COMPASS in structuring meiotic chromosomes in the germline of C. elegans. Inactivation of SET-2, the C. elegans homologue of the catalytic subunit SET1, strongly enhanced chromosome organization defects and loss of fertility resulting from partial depletion of condensin-II. Loss of CFP-1, the chromatin targeting subunit of COMPASS, similarly affected germline chromatin compaction measured by FLIM-FRET and enhanced condensin-II knock-down phenotypes. Defects in chromosome morphology following conditional inactivation of topoisomerase II, another structural component of chromosomes, were also aggravated in the absence of set-2. Our results are consistent with a role of SET1/COMPASS in shaping meiotic chromosomes in the C. elegans germline, and have important implications for how chromatin-modifying complexes and histone modifications may cooperate with non histone-proteins to achieve proper chromosome organization, not only in meiosis, but also in mitosis.

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Chromatin conformation and transcriptional activity are permissive regulators of DNA replication initiation in Drosophila

Project description:We replaced the endogenous histones of Drosophila melanogaster with either histones containing an H3K9R mutation or histones containing an H4K16R mutation to interrogate established genome-wide correlations between chromatin state, transcription, and DNA replication timing. We performed total RNA-seq in H4K16R males and females to investigate the role of H4K16 in dosage compensation of the male X chromosome. We found that H4K16 directly promotes hyper-expression of the male X chromosome in Drosophila. To generate replication timing profiles, we performed Repli-seq in HWT males and females, H4K16R males and females, and H3K9R females. We found that H3K9 promotes late replication of the pericentromeric heterochromatin and H4K16 promotes early replication of the male X chromosome.

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Project description:no germline males vs reference

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