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Enrichment of H3K9me2 on unsynapsed chromatin in C. elegans does not target de novo sites [RNA-Seq]

ABSTRACT: We sequenced mRNA isolated from adult hermaphrodite met-2;him-8 and him-8 gonads in order to determine the gene expression profile of germ cells with or without H3K9me2.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE67029 | GEO | 2015/09/04

SECONDARY ACCESSION(S): PRJNA278751

REPOSITORIES: GEO

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Enrichment of H3K9me2 on unsynapsed chromatin in C. elegans does not target de novo sites [RNA-Seq]

Project description:We sequenced mRNA isolated from adult hermaphrodite met-2;him-8 and him-8 gonads in order to determine the gene expression profile of germ cells with or without H3K9me2. Examination of mRNA profiles in nematode gonad of met-2;him-8 (without H3K9me2) and him-8 (with H3K9me2)

2015-09-04 | E-GEOD-67029 | biostudies-arrayexpress

Enrichment of H3K9me2 on unsynapsed chromatin in C. elegans does not target de novo sites [ChIP-Seq]

Project description:Characterization of the H3K9me2 distribution in the C. elegans adult hermaphrodite genome using ChIP-Seq

2015-09-04 | GSE67028 | GEO

Enrichment of H3K9me2 on unsynapsed chromatin in C. elegans does not target de novo sites [ChIP-Seq]

Project description:Characterization of the H3K9me2 distribution in the C. elegans adult hermaphrodite genome using ChIP-Seq Examination of H3K9me2 in two different nematode strains: fer-1 control and fer-1;him-8 mutant, where the X chromosomes are unsynapsed. The fer-1 mutation prevents production of embryos.

2015-09-04 | E-GEOD-67028 | biostudies-arrayexpress

Enrichment of H3K9me2 on Unsynapsed Chromatin in Caenorhabditis elegans Does Not Target de Novo Sites.

Project description:Many organisms alter the chromatin state of unsynapsed chromosomes during meiotic prophase, a phenomenon hypothesized to function in maintaining germline integrity. In Caenorhabditis elegans, histone H3 lysine 9 dimethylation (H3K9me2) is detected by immunolabeling as enriched on unsynapsed meiotic chromosomes. Loss of the SET domain protein, MET-2, greatly reduces H3K9me2 abundance and results in germline mortality. Here, we used him-8 mutations to disable X chromosome synapsis and performed a combination of molecular assays to map the sites of H3K9me2 accumulation, evaluate H3K9me2 abundance in germline vs. whole animals, and evaluate the impact of H3K9me2 loss on the germline transcriptome. Our data indicate that H3K9me2 is elevated broadly across the X chromosome and at defined X chromosomal sites in him-8 adults compared with controls. H3K9me2 levels are also elevated to a lesser degree at sites on synapsed chromosomes in him-8 adults compared with controls. These results suggest that MET-2 activity is elevated in him-8 mutants generally as well as targeted preferentially to the unsynapsed X. Abundance of H3K9me2 and other histone H3 modifications is low in germline chromatin compared with whole animals, which may facilitate genome reprogramming during gametogenesis. Loss of H3K9me2 has a subtle impact on the him-8 germline transcriptome, suggesting H3K9me2 may not be a major regulator of developmental gene expression in C. elegans. We hypothesize H3K9me2 may have a structural function critical for germline immortality, and a greater abundance of these marks may be required when a chromosome does not synapse.

| S-EPMC4555223 | biostudies-literature

Enrichment of H3K9me2 on unsynapsed chromatin in C. elegans does not target de novo sites

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

2015-09-04 | GSE67030 | GEO

Enrichment of H3K9me2 on unsynapsed chromatin in C. elegans does not target de novo sites

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

2015-09-04 | E-GEOD-67030 | biostudies-arrayexpress

Genomic distribution of H3K9me2 in wild-type vs. arle-14 mutant C. elegans embryos

Project description:We discovered arle-14/B0336.5 as a critical gene for H3K9 di-methylation. To test the hypothesis that ARLE-14 targets the H3K9 methyltransferase MET-2 to specific loci, we compared the distribution of H3K9me2 in wild-type and arle-14 mutants by ChIP-Seq. Our results reveal that H3K9me2 genomic distribution is similar in wild-type vs. mutants and ARLE-14 is not required for targeting MET-2.

2018-08-22 | GSE113841 | GEO

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.

2019-02-06 | GSE122339 | GEO

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

2019-02-06 | GSE122335 | GEO

XOL-1 regulates developmental timing by modulating the H3K9 landscape in C. elegans early embryos

Project description:Sex determination in the nematode C. elegans is controlled by the master regulator XOL-1 during embryogenesis. Expression of xol-1 is dependent on the ratio of X chromosomes and autosomes, which differs between XX hermaphrodites and XO males. In males, xol-1 is highly expressed and in hermaphrodites, xol-1 is expressed at very low levels. XOL-1 activity is known to be critical for the proper development of C. elegans males, but its low expression was considered to be of minimal importance in the development of hermaphrodite embryos. Our study reveals that XOL-1 plays an important role as a regulator of developmental timing during hermaphrodite embryogenesis. Using a combination of imaging and bioinformatics techniques, we found that hermaphrodite embryos have an accelerated rate of cell division, as well as a more developmentally advanced transcriptional program when xol-1 is lost. Further analyses reveal that XOL-1 is responsible for regulating the timing of initiation of dosage compensation on the X chromosomes, and the appropriate expression of sex-biased transcriptional programs in hermaphrodites. We found that xol-1 mutant embryos overexpress the H3K9 methyltransferase met-2 and have an altered H3K9me landscape. Some of these effects of the loss of xol-1 gene were reversed by the loss of met-2. These findings demonstrate that XOL-1 plays an important role as a developmental regulator in embryos of both sexes, and that MET-2 acts as a downstream effector of XOL-1 activity in hermaphrodites.

2024-08-05 | GSE262626 | GEO

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