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Regulation of MORC-1 is key to the CSR-1-mediated germline gene licensing mechanism in C. elegans

ABSTRACT: Regulation of MORC-1 is key to the CSR-1-mediated germline gene licensing mechanism in C. elegans

PROVIDER: PRJNA1072655 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27848624.fastq.gz	Fastqsanger.gz
	SRR27848625.fastq.gz	Fastqsanger.gz
	SRR27848626.fastq.gz	Fastqsanger.gz
	SRR27848627.fastq.gz	Fastqsanger.gz
	SRR27848628.fastq.gz	Fastqsanger.gz

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Regulation of MORC-1 is key to the CSR-1-mediated germline gene licensing mechanism in C. elegans

Project description:The Argonaute CSR-1 is essential for germline development in C. elegans. Loss of CSR-1 leads to the downregulation of thousands of germline-expressed genes, supporting a model in which CSR-1 “licenses” gene expression via a poorly understood mechanism. In contrast, a small subset of genes is upregulated in csr-1 mutants, including morc-1, which encodes a conserved GHKL-type ATPase. We show that morc-1 is overexpressed in csr-1 mutants and accumulates over CSR-1 licensed targets, coinciding with aberrant gain of H3K9me3, reduced H3K36me3, and transcriptional repression. Strikingly, loss of morc-1 fully rescues these chromatin defects and partially restores gene expression and fertility in csr-1 mutants. Conversely, ectopic overexpression of MORC-1 in the wild-type germline is sufficient to repress CSR-1 licensed targets and severely compromise fertility. These findings support a model in which CSR-1 prevents MORC-1 overexpression and consequent misregulation of CSR-1 licensed genes.

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