Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Two parallel pathways recruit the H3K9me3 HMT in somatic cells, requiring the Argonaut NRDE-3, or the MBT-domain protein, LIN-61 (RNA-seq)

ABSTRACT: The establishment and maintenance of chromatin domains shape the epigenetic memory of a cell, with histone H3 lysine 9 methylation defining repressed heterochromatin. We show that in C. elegans the SET-25 (SUV39/G9a) HMT that catalyzes H3K9me1-3, is able to establish repressed domains de novo. We identify here two distinct pathways that recruit SET-25 to its targets. One requires LIN-61 (L3MBTL2), a conserved protein with 4 MBT domains that recognizes H3K9me2 deposited by the HMT MET-2 (SETDB1). The second pathway is MET-2-independent and requires a somatic Argonaut NRDE-3 and 22nt small nuclear RNAs. This NRDE-3 pathway targets ~10% of all SET-25-modified loci genome-wide including intact RNA and DNA transposons. Removal of both pathways in the met-2;nrde-3 double mutant synergistically derepresses transposons in early embryos and elevates embryonic lethality. The redundancy of these pathways illustrates the key role played by chromatin-mediated silencing in protecting the genome against inherent threats.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE156549 | GEO | 2020/12/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Two parallel pathways recruit the H3K9me3 HMT in somatic cells, requiring the Argonaut NRDE-3, or the MBT-domain protein, LIN-61 (ChIP-seq)

Project description:The establishment and maintenance of chromatin domains shape the epigenetic memory of a cell, with histone H3 lysine 9 methylation defining repressed heterochromatin. We show that in C. elegans the SET-25 (SUV39/G9a) HMT that catalyzes H3K9me1-3, is able to establish repressed domains de novo. We identify here two distinct pathways that recruit SET-25 to its targets. One requires LIN-61 (L3MBTL2), a conserved protein with 4 MBT domains that recognizes H3K9me2 deposited by the HMT MET-2 (SETDB1). The second pathway is MET-2-independent and requires a somatic Argonaut NRDE-3 and 22nt small nuclear RNAs. This NRDE-3 pathway targets ~10% of all SET-25-modified loci genome-wide including intact RNA and DNA transposons. Removal of both pathways in the met-2;nrde-3 double mutant synergistically derepresses transposons in early embryos and elevates embryonic lethality. The redundancy of these pathways illustrates the key role played by chromatin-mediated silencing in protecting the genome against inherent threats.

2020-12-01 | GSE156548 | GEO

Two parallel pathways recruit the H3K9me3 HMT in somatic cells, requiring the Argonaut NRDE-3, or the MBT-domain protein, LIN-61 (smallRNA-seq)

2020-12-01 | GSE156550 | GEO

Distinct regulatory mechanisms by the nuclear Argonautes HRDE-1 and NRDE-3 in the soma of Caenorhabditis elegans.

Project description:Histone H3 lysine 9 methylation (H3K9me) and nuclear RNAi are two processes with roles in repression of repetitive elements and regulation of gene expression. Recently, they were also implicated in dosage compensation, a mechanism that accommodates for the differences in gene dosage between the biological sexes. In Caenorhabditis elegans, dosage compensation is achieved via epigenetic modifications on both X chromosomes of hermaphrodites, effectively dampening their expression by half to match the single X chromosome in males. This chromosome-wide process also relies on the anchoring and compaction of the X chromosomes near the nuclear lamina, mediated by the H3K9 histone methyltransferases MET-2, SET-25 and SET-32. H3K9me is also involved in gene silencing during nuclear RNAi, and recent evidence suggests that mutations in the nuclear RNAi machinery impact X chromosome compaction and dosage compensation. The nuclear Argonautes HRDE-1 and NRDE-3 are responsible for the recruitment of the H3K9 histone methyltransferases to targets in the germline and the soma, respectively, during nuclear RNAi. We investigated the impact of the loss of nuclear Argonautes and/or H3K9 methyltransferases on both dosage compensation and global gene expression during somatic development. Our immunofluorescence and bioinformatic analyses suggest that the nuclear RNAi and H3K9me pathways are involved in the packaging of the X chromosomes during dosage compensation, without consequence to their transcriptional output. Instead, mutant RNAi mutants exhibit global transcriptional differences, in which HRDE-1 and NRDE-3 affect expression of their native targets through different modes of regulation and different relationships between each nuclear Argonaute and H3K9 methylation.

2024-10-01 | GSE277005 | GEO

Two parallel pathways recruit the H3K9me3 HMT in somatic cells, requiring the Argonaut NRDE-3, or the MBT-domain protein, LIN-61

Project description:Two parallel pathways recruit the H3K9me3 HMT in somatic cells, requiring the Argonaut NRDE-3, or the MBT-domain protein, LIN-61

| PRJNA658324 | ENA

H3K9me2 and BRCA1 cooperate to prevent satellite repeat transcription, R-loop formation and germline sterility [RNA-seq]

Project description:Repetitive sequences, transposable elements and silent tissue-specific genes in C. elegans are differentially enriched for di- and tri-methyl H3 lysine 9 (H3K9). SET-25 (SUV39h1/h2) catalyzes H3K9me3, while MET-2 (SetDB1) deposits only H3K9me1/me2. RNA-seq and genome-wide H3K9 methylation mapping in met-2 and set-25 single mutants showed that H3K9me2-mediated repression of satellite repeats by MET-2 correlates with germline integrity. Aberrant transcription of repeats and DNA transposons generates R-loops, loss of fertility and hydroxyurea hypersensitivity. In a genome-wide synthetic lethal screen, we identified the BRCA1 complex and factors implicated in the degradation of nuclear RNA as essential for germline integrity in met-2 mutants. Highly additive with met-2, the loss of the BRCA1 complex triggers satellite repeat transcription, generating R-loops on transcribed repeats. Supporting direct causality between satellite repeat transcription and BRCA1-mediated genome integrity, the targeted induction of MSAT1 transcripts at endogenous sites leads to damage-induced loss of fertility in wild-type C. elegans.

2017-07-04 | GSE100723 | GEO

H3K9me2 and BRCA1 cooperate to prevent satellite repeat transcription, R-loop formation and germline sterility [ChIP-seq]

2017-07-04 | GSE100724 | GEO

Two parallel pathways recruit the H3K9me3 HMT in somatic cells, requiring the Argonaut NRDE-3, or the MBT-domain protein, LIN-61 (ChIP-seq)

Project description:Two parallel pathways recruit the H3K9me3 HMT in somatic cells, requiring the Argonaut NRDE-3, or the MBT-domain protein, LIN-61 (ChIP-seq)

| PRJNA658328 | ENA

Two parallel pathways recruit the H3K9me3 HMT in somatic cells, requiring the Argonaut NRDE-3, or the MBT-domain protein, LIN-61 (smallRNA-seq)

Project description:Two parallel pathways recruit the H3K9me3 HMT in somatic cells, requiring the Argonaut NRDE-3, or the MBT-domain protein, LIN-61 (smallRNA-seq)

| PRJNA658330 | ENA

Two parallel pathways recruit the H3K9me3 HMT in somatic cells, requiring the Argonaut NRDE-3, or the MBT-domain protein, LIN-61 (RNA-seq)

Project description:Two parallel pathways recruit the H3K9me3 HMT in somatic cells, requiring the Argonaut NRDE-3, or the MBT-domain protein, LIN-61 (RNA-seq)

| PRJNA658329 | ENA

Nanosynbacter sp. HMT-352

Project description:Nanosynbacter sp. HMT-352 Genome Sequencing and Assembly

| PRJNA784561 | ENA