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Drosophila melanogaster

ABSTRACT: Linker histone H1 prevents R-loop accumulation and genome instability in heterochromatin [ChIP Seq]

PROVIDER: PRJNA386953 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5572460.fastq.gz	Fastqsanger.gz
	SRR5572461.fastq.gz	Fastqsanger.gz
	SRR5572462.fastq.gz	Fastqsanger.gz
	SRR5572463.fastq.gz	Fastqsanger.gz
	SRR5572464.fastq.gz	Fastqsanger.gz

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Novel roles of C. elegans heterochromatin protein HP1 and linker histone HIS-24 in the regulation of innate immune gene expression and stress Response

Project description:Linker histone H1 and heterochromatin protein 1 (HP1) are essential components ofheterochromatin which contribute to the transcriptional repression of genes. It has been shown that the methylation mark on the histone H1 serves as a specific recognition code for the chromodomain of HP1, however, the functional role of the HP1/H1 complex remains elusive. Using C. elegans, we elucidate the function of the linker histone variant HIS-24 and heterochromatin proteins HPL/HP1 in the cooperative transcriptional regulation of immunerelevant and stress resistance genes. We also show that HIS-24 and HPL act redundantly in vulval cell fate specification and gonad development. Finally, we provide the first evidence that HPL-1 interacts with HIS-24 at mono-methylated lysine 14 and associates in vivo with promoters of infection-inducible genes: the caenacin (cnc)- and the thaumatin (thn)- gene clusters. Our results highlight a functional link between epigenetic regulation by HP1/H1 the innate immune system and stress response. The experiment was performed using biological independent replicates of pooled worms. For the KO mutants we used duplicates and for WT condition quadruplicates.

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The histone variant H2A.W and linker histone H1 co-regulate heterochromatin accessibility and DNA methylation

Project description:In flowering plants, heterochromatin is demarcated by the histone variant H2A.W, elevated levels of the linker histone H1, and specific epigenetic modifications, such as high levels of DNA methylation at both CG and non-CG sites. How H2A.W regulates heterochromatin organization and interacts with other heterochromatic features is unclear. Here, we create an h2a.w null mutant via CRISPR-Cas9, h2a.w-2, to analyze the in vivo function of H2A.W. We find that H2A.W antagonizes deposition of H1 at heterochromatin and that non-CG methylation and accessibility are moderately decreased in h2a.w-2 heterochromatin. Compared to H1 loss alone, combined loss of H1 and H2A.W greatly increases accessibility and facilitates non-CG DNA methylation in heterochromatin, suggesting co-regulation of heterochromatic features by H2A.W and H1. Our results suggest that H2A.W helps maintain optimal heterochromatin accessibility and DNA methylation by promoting chromatin compaction together with H1, while also inhibiting excessive H1 incorporation.

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