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

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

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE144253 | GEO | 2020/04/21

REPOSITORIES: GEO

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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.

| S-EPMC7261013 | biostudies-literature

Histone H3K9 methylation promotes formation of genome compartments in C. elegans via chromosome compaction and perinuclear anchoring (ChIP-seq)

Project description:Genomic regions preferentially associate with regions of similar transcriptional activity, partitioning genomes into active and inactive compartments within the nucleus. Here we explored mechanisms controlling genome compartment organization in C. elegans and investigated roles for compartments in regulating gene expression. The distal arms of C. elegans chromosomes, which are enriched for heterochromatic histone modifications including H3K9me, interact with each other both in cis and in trans, while interacting less frequently with central regions of chromosomes, 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 genome 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 that are established by the dosage-compensation condensin complex. Our results demonstrate that H3K9me plays crucial roles in regulating genome organization at multiple levels.

2020-04-21 | GSE144251 | GEO

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

Project description:Genomic regions preferentially associate with regions of similar transcriptional activity, partitioning genomes into active and inactive compartments within the nucleus. Here we explored mechanisms controlling genome compartment organization in C. elegans and investigated roles for compartments in regulating gene expression. The distal arms of C. elegans chromosomes, which are enriched for heterochromatic histone modifications including H3K9me, interact with each other both in cis and in trans, while interacting less frequently with central regions of chromosomes, 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 genome 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 that are established by the dosage-compensation condensin complex. Our results demonstrate that H3K9me plays crucial roles in regulating genome organization at multiple levels.

2020-04-21 | GSE144252 | GEO

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

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

| PRJNA603164 | ENA

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

Project description:Histone H3K9 methylation promotes formation of genome compartments in C. elegans via chromosome compaction and perinuclear anchoring (Hi-C)

| PRJNA603165 | ENA

Histone H3K9 methylation promotes formation of genome compartments in C. elegans via chromosome compaction and perinuclear anchoring (ChIP-seq)

Project description:Histone H3K9 methylation promotes formation of genome compartments in C. elegans via chromosome compaction and perinuclear anchoring (ChIP-seq)

| PRJNA603166 | ENA

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.

2015-12-11 | GSE74134 | GEO

Loss of H3K9 trimethylation alters chromosome compaction and transcription factor retention during mitosis.

Project description:Recent studies have shown that repressive chromatin machinery, including DNA methyltransferases and polycomb repressor complexes, binds to chromosomes throughout mitosis and their depletion results in increased chromosome size. In the present study, we show that enzymes that catalyze H3K9 methylation, such as Suv39h1, Suv39h2, G9a and Glp, are also retained on mitotic chromosomes. Surprisingly, however, mutants lacking histone 3 lysine 9 trimethylation (H3K9me3) have unusually small and compact mitotic chromosomes associated with increased histone H3 phospho Ser10 (H3S10ph) and H3K27me3 levels. Chromosome size and centromere compaction in these mutants were rescued by providing exogenous first protein lysine methyltransferase Suv39h1 or inhibiting Ezh2 activity. Quantitative proteomic comparisons of native mitotic chromosomes isolated from wild-type versus Suv39h1/Suv39h2 double-null mouse embryonic stem cells revealed that H3K9me3 was essential for the efficient retention of bookmarking factors such as Esrrb. These results highlight an unexpected role for repressive heterochromatin domains in preserving transcription factor binding through mitosis and underscore the importance of H3K9me3 for sustaining chromosome architecture and epigenetic memory during cell division.

| S-EPMC10113154 | biostudies-literature

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

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

2019-02-06 | GSE122341 | GEO