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An unstructured MET-2/SETDB1 cofactor ensures H3K9me2, focus formation and perinuclear anchoring

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE122341 | GEO | 2019/02/06

REPOSITORIES: GEO

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An unstructured MET-2/SETDB1 cofactor ensures H3K9me2, focus formation and perinuclear anchoring [RNA-seq]

Project description:The segregation of the genome into accessible euchromatin and histone H3 lysine 9 methylated (H3K9me) heterochromatin is essential for the repression of repetitive elements and tissue-specific genes. In C. elegans, the SETDB1 homolog MET-2 catalyzes H3K9me1 and me2. In worms as in vertebrates, the regulation of this crucial enzyme remains enigmatic. Contrary to the localization of overexpressed MET-2, we find endogenous MET-2 to be nuclear throughout development, enriched in perinuclear foci in a cell cycle-dependent manner. We show by mass spectrometry that MET-2 associates with a highly unstructured protein, LIN-65, and a conserved GTPase effector ARLE-14. All three colocalize at heterochromatic foci. Ablation of lin-65, but not arle-14, mislocalizes and destabilizes MET-2, resulting in decreased H3K9me2, derepression of MET-2 targets, and loss of fertility. Importantly, mutation of met-2 or lin-65 is sufficient to disrupt the perinuclear clustering of heterochromatin genome-wide. Thus, LIN-65 is an essential cofactor of MET-2 required for H3K9me2 deposition, heterochromatin clustering, perinuclear anchoring, and transcriptional repression.

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An unstructured MET-2/SETDB1 cofactor ensures H3K9me2, focus formation and perinuclear anchoring [ChIP-seq]

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An unstructured MET-2/SETDB1 cofactor ensures H3K9me2, focus formation and perinuclear anchoring

Project description:An unstructured MET-2/SETDB1 cofactor ensures H3K9me2, focus formation and perinuclear anchoring

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An unstructured MET-2/SETDB1 cofactor ensures H3K9me2, focus formation and perinuclear anchoring [RNA-seq]

Project description:An unstructured MET-2/SETDB1 cofactor ensures H3K9me2, focus formation and perinuclear anchoring [RNA-seq]

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An unstructured MET-2/SETDB1 cofactor ensures H3K9me2, focus formation and perinuclear anchoring [ChIP-seq]

Project description:An unstructured MET-2/SETDB1 cofactor ensures H3K9me2, focus formation and perinuclear anchoring [ChIP-seq]

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Heterochromatic foci and transcriptional repression by an unstructured MET-2/SETDB1 co-factor LIN-65.

Project description:The segregation of the genome into accessible euchromatin and histone H3K9-methylated heterochromatin helps silence repetitive elements and tissue-specific genes. In Caenorhabditis elegans, MET-2, the homologue of mammalian SETDB1, catalyzes H3K9me1 and me2, yet like SETDB1, its regulation is enigmatic. Contrary to the cytosolic enrichment of overexpressed MET-2, we show that endogenous MET-2 is nuclear throughout development, forming perinuclear foci in a cell cycle-dependent manner. Mass spectrometry identified two cofactors that bind MET-2: LIN-65, a highly unstructured protein, and ARLE-14, a conserved GTPase effector. All three factors colocalize in heterochromatic foci. Ablation of lin-65, but not arle-14, mislocalizes and destabilizes MET-2, resulting in decreased H3K9 dimethylation, dispersion of heterochromatic foci, and derepression of MET-2 targets. Mutation of met-2 or lin-65 also disrupts the perinuclear anchoring of genomic heterochromatin. Loss of LIN-65, like that of MET-2, compromises temperature stress resistance and germline integrity, which are both linked to promiscuous repeat transcription and gene expression.

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Histone H3K9 methylation promotes formation of genome compartments in Caenorhabditis elegans via chromosome compaction and perinuclear anchoring.

Project description:Genomic regions preferentially associate with regions of similar transcriptional activity, partitioning genomes into active and inactive compartments within the nucleus. Here we explore mechanisms controlling genome compartment organization in Caenorhabditis elegans and investigate roles for compartments in regulating gene expression. Distal arms of C. elegans chromosomes, which are enriched for heterochromatic histone modifications H3K9me1/me2/me3, interact with each other both in cis and in trans, while interacting less frequently with central regions, leading to genome compartmentalization. Arms are anchored to the nuclear periphery via the nuclear envelope protein CEC-4, which binds to H3K9me. By performing genome-wide chromosome conformation capture experiments (Hi-C), we showed that eliminating H3K9me1/me2/me3 through mutations in the methyltransferase genes met-2 and set-25 significantly impaired formation of inactive Arm and active Center compartments. cec-4 mutations also impaired compartmentalization, but to a lesser extent. We found that H3K9me promotes compartmentalization through two distinct mechanisms: Perinuclear anchoring of chromosome arms via CEC-4 to promote their cis association, and an anchoring-independent mechanism that compacts individual chromosome arms. In both met-2 set-25 and cec-4 mutants, no dramatic changes in gene expression were found for genes that switched compartments or for genes that remained in their original compartment, suggesting that compartment strength does not dictate gene-expression levels. Furthermore, H3K9me, but not perinuclear anchoring, also contributes to formation of another prominent feature of chromosome organization, megabase-scale topologically associating domains on X established by the dosage compensation condensin complex. Our results demonstrate that H3K9me plays crucial roles in regulating genome organization at multiple levels.

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Histone H3K9 methylation promotes formation of genome compartments in C. elegans via chromosome compaction and perinuclear anchoring

Project description:This SuperSeries is composed of the SubSeries listed below.

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Perinuclear anchoring of H3K9-methylated chromatin stabilizes induced cell fate

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-12-11 | E-GEOD-74134 | biostudies-arrayexpress

Perinuclear anchoring of H3K9-methylated chromatin stabilizes induced cell fate

Project description:This SuperSeries is composed of the SubSeries listed below.

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