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

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

PROVIDER: PRJNA601803 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10906500.fastq.gz	Fastqsanger.gz
	SRR10906496.fastq.gz	Fastqsanger.gz
	SRR10906497.fastq.gz	Fastqsanger.gz
	SRR10906498.fastq.gz	Fastqsanger.gz
	SRR10906499.fastq.gz	Fastqsanger.gz

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C. elegans establishes germline versus soma by balancing inherited histone methylation

Project description:C. elegans establishes germline versus soma by balancing inherited histone methylation

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

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

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

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.

2020-01-17 | GSE143837 | GEO

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

2020-01-17 | GSE143838 | GEO

<i>Caenorhabditis elegans</i> establishes germline versus soma by balancing inherited histone methylation.

Project description:Formation of a zygote is coupled with extensive epigenetic reprogramming to enable appropriate inheritance of histone methylation and prevent developmental delays. In Caenorhabditis elegans, this reprogramming is mediated by the H3K4me2 demethylase SPR-5 and the H3K9 methyltransferase, MET-2. In contrast, the H3K36 methyltransferase MES-4 maintains H3K36me2/3 at germline genes between generations to facilitate re-establishment of the germline. To determine whether the MES-4 germline inheritance pathway antagonizes spr-5; met-2 reprogramming, we examined the interaction between these two pathways. We found that the developmental delay of spr-5; met-2 mutant progeny is associated with ectopic H3K36me3 and the ectopic expression of MES-4-targeted germline genes in somatic tissues. Furthermore, the developmental delay is dependent upon MES-4 and the H3K4 methyltransferase, SET-2. We propose that MES-4 prevents crucial germline genes from being repressed by antagonizing maternal spr-5; met-2 reprogramming. Thus, the balance of inherited histone modifications is necessary to distinguish germline versus soma and prevent developmental delay.This article has an associated 'The people behind the papers' interview.

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C. elegans establishes germline versus soma by balancing inherited histone methylation

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

2020-01-17 | GSE143839 | GEO

Drosophila TRAP soma vs germline

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Soma-to-Germline miRNA inheritance via Yolk Promotes Stress Resilience in Progeny [mRNA]

Project description:At the onset of reproduction, oviparous animals synthesize large amounts of yolk in somatic tissues to provide lipids and other nutrients to their progeny. However, whether the yolk transports other types of molecules, such as RNAs with gene regulatory functions, remains largely unexplored. Here, we have biochemically purified the yolk in the nematode Caenorhabditis elegans and show it contains microRNAs (miRNAs). We provide evidence that the yolk transports such miRNAs from the mother’s intestine to the embryos via the lipoprotein yolk receptor RME-2. These yolk-enriched miRNAs inherited by the embryos regulate the transcriptomes of developing larvae. Moreover, environmental stresses and maternal age modulate the transfer of yolk-enriched miRNAs, providing stress resilience benefits to progeny. This discovery establishes a novel paradigm in intergenerational gene regulation, where the gut-germline axis orchestrates the transmission of environmental cues through yolk-enriched miRNAs. Our work reveals a new mechanism underlying the soma-to-germline transfer of epigenetic information in animals.

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Soma-to-Germline miRNA inheritance via Yolk Promotes Stress Resilience in Progeny [small RNA]

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SCML2 Establishes the Male Germline Epigenome

Project description:Gametogenesis is dependent on the expression of germline-specific genes. However, it remains unknown how the germline epigenome is distinctly established from that of somatic lineages. Here we show that genes commonly expressed in somatic lineages and spermatogenesis-progenitor cells undergo repression in a genome-wide manner in late stages of the male germline and identify underlying mechanisms. SCML2, a germline-specific subunit of a Polycomb repressive complex 1 (PRC1), establishes the unique epigenome of the male germline through two distinct antithetical mechanisms. SCML2 works with PRC1 and promotes RNF2-dependent ubiquitination of H2A, thereby marking somatic/progenitor genes on autosomes for repression. Paradoxically, SCML2 also prevents RNF2-dependent ubiquitination of H2A on sex chromosomes during meiosis, thereby enabling unique epigenetic programming of sex chromosomes for male reproduction. Our results reveal divergent mechanisms involving a shared regulator by which the male germline epigenome is distinguished from that of the soma and progenitor cells.

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