Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Failure to maternally reprogram histone methylation causes developmental delay due to germline transcription in somatic tissues

ABSTRACT: Failure to maternally reprogram histone methylation causes developmental delay due to germline transcription in somatic tissues

PROVIDER: PRJNA635566 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11862546_1.fastq.gz	Fastqsanger.gz
	SRR11862546_2.fastq.gz	Fastqsanger.gz
	SRR11862547_1.fastq.gz	Fastqsanger.gz
	SRR11862547_2.fastq.gz	Fastqsanger.gz
	SRR11862548_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Failure to maternally reprogram histone methylation causes developmental delay due to germline transcription in somatic tissues

Project description:In C. elegans, the H3K4me2 demethylase, SPR-5, and the H3K9 methyltransferase, MET-2, are maternally deposited into the oocyte where they reprogram histone methylation to prevent somatic expression of germline genes. Here, we show that the progeny of spr-5; met-2 mutants display a severe developmental delay that is associated with the ectopic expression of germline genes targeted by the H3K36me2/3 methyltransferase, MES-4. Maternally deposited MES-4 maintains H3K36me2/3 at a subset of germline genes (hereafter referred to as MES-4 germline genes) in a transcription-independent manner, and this is required for germline proliferation in the subsequent generation. By performing ChIP-seq on L1 progeny from spr-5; met-2 mutants, we find that MES-4 germline genes ectopically accumulate H3K36me3 in somatic tissues. Additionally, knocking down MES-4 suppresses the ectopic expression of MES-4 germline genes and rescues the developmental delay. These data suggest a model where SPR-5, MET-2 and MES-4 carefully balance the inheritance of histone methylation from the parental germline to ensure the proper specification of germline versus soma in the progeny. Without SPR-5; MET-2 maternal reprogramming, somatic cells struggle to specify their proper cell fate amongst the background noise of inappropriate germline gene transcription, leading to a severe developmental delay.

2020-05-29 | GSE151340 | GEO

LSD1 functions through CoREST to maternally reprogram histone methylation

Project description:LSD1 functions through CoREST to maternally reprogram histone methylation

| PRJNA705990 | ENA

Maternally deposited germline piRNAs silence the tirant retrotransposon in somatic cells

Project description:Transposable elements (TEs), whose propagation can result in severe damage to the host genome, are silenced in the animal gonad by Piwi-interacting RNAs (piRNAs). piRNAs produced in the ovaries are deposited in the embryonic germline and initiate TE repression in the germline progeny. Whether the maternally transmitted piRNAs play a role in the silencing of somatic TEs is, however, unknown. Here we show that maternally transmitted piRNAs from the tirant retrotransposon in Drosophila are required for the somatic silencing of the TE and correlate with an increase in histone H3K9 trimethylation an active tirant copy. Comparison of tirant piRNAs in two Drosophila simulans natural populations.

2013-04-09 | E-GEOD-40592 | biostudies-arrayexpress

Maternally deposited germline piRNAs silence the tirant retrotransposon in somatic cells

2013-04-09 | GSE40592 | GEO

C. elegans establishes germline versus soma by balancing inherited histone methylation [ChIP-seq]

2020-01-17 | GSE143838 | GEO

C. elegans establishes germline versus soma by balancing inherited histone methylation [RNA-seq]

2020-01-17 | GSE143837 | GEO

Reprogram-seq

Project description:Reprogram-seq

| PRJNA1056273 | ENA

Reduction in Cord Blood Graft Potency Due to Processing Delay Can be Prevented by Trehalose Supplementation

Project description:Reduction in Cord Blood Graft Potency Due to Processing Delay Can be Prevented by Trehalose Supplementation

| PRJNA1235136 | ENA

Maternally inherited piRNAs silence transposons during Drosophila embryogenesis

Project description:The piRNA pathway controls transposon expression in animal germ cells, thereby ensuring genome stability over generations. piRNAs are maternally deposited and required for proper transposon silencing in adult offspring. However, a long-standing question in the field is the precise function of maternally deposited piRNAs and its associated factors during embryogenesis. Here, we probe the spatio-temporal expression patterns of several piRNA pathway components during early stages of development. Amongst those, factors required for transcriptional gene silencing (TGS) showed ubiquitous abundance in somatic and pole cells throughout the first half of embryogenesis. We further analysed the transcriptomes of various embryo stages and correlated these with the presence of selected chromatin marks. We found that a number of transposon families show bursts of transcription during early embryonic stages. Transposons heavily targeted by maternally deposited piRNAs accumulated repressive chromatin marks following their spike in expression. Furthermore, depletion of maternally deposited Piwi protein in early embryos resulted in increased expression of transposons targeted by inherited piRNAs and was accompanied by a strong loss of repressive chromatin marks at coding sequences. Overall, our data suggests a pivotal role for the piRNA pathway in transposon defence during Drosophila embryogenesis in somatic cells.

2021-07-26 | PXD022409 | Pride

Maternally deprived epigenome

Project description:Genome-wide 5mC and 5hmC DNA profile of the hippocampus of maternally deprived rats

| PRJEB21695 | ENA