The germline-specific factor OEF-1 facilitates coordinated progression through germ cell development in C. elegans
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PROVIDER: PRJNA419235 | ENA |
REPOSITORIES: ENA
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Project description:How germ cells faithfully pass genetic material to the next generation despite undergoing several developmental transitions during maturation is poorly understood. Here we identify a novel factor in C. elegans, OEF-1, that is highly germline-specific, with early expression in the embryonic germ lineage and differential expression in larvae and adults depending on the gametogenesis program. OEF-1 is nuclear and associates with autosomal germline-expressed genes. Loss of OEF-1 triggers accelerated germ cell progression, leading to defects at multiple points during germline development. Thus OEF-1 may act to coordinate the timely progression of germ cells through proliferation, meiotic entry, and gametogenesis.
2017-11-22 | GSE107190 | GEO
Project description: Not available
| S-EPMC5788521 | biostudies-literature
Project description:This SuperSeries is composed of the following subset Series: GSE35775: The H3K27 demethylase Utx facilitates somatic and germ cell epigenetic reprogramming to pluripotency [Affymetrix gene expression] GSE37821: The H3K27 demethylase Utx facilitates somatic and germ cell epigenetic reprogramming to pluripotency [ChIP-Seq] Refer to individual Series
2012-05-29 | E-GEOD-37822 | biostudies-arrayexpress
Project description:Sex-determining chromosomes exhibit complex global regulation in germ cells, in part due to the absence of dosage compensatory mechanisms found in the soma. In the XX hermaphrodite germ line of C. elegans, the X chromosome houses few germline-expressed genes [1] and is poorly expressed, though not completely silent, through most of germ cell development [2]. A chromatin-modifying pathway consisting of the histone methyltransferase (HMT) MES-4 and the Polycomb Repressive Complex 2 (PRC2) orthologs MES-2/3/6 contributes to X silencing in C. elegans germ cells [3-5]. MES-4 promotes H3K36me3 accumulation on autosomes, which leads to concentration of H3K27me3 on the X by MES-2/3/6 [5]. Loss of MES activity results in inappropriate activation of X-linked genes and second-generation sterility [5, 6]. The two marks occupy mutually exclusive domains of the genome [5, 7], leading to a model in which the presence of one modification prevents the accumulation of the other at specific loci. However, further details about how this repulsion mechanism between H3K27me3 and H3K36me3 is established remain mysterious. Here we implicate the zinc-finger protein OEF-1 in counterbalancing the accumulation of H3K27me3 throughout the genome, particularly on the X chromosome. Strikingly OEF-1, like MES-4, is localized to sites of active gene expression in the germ line, and promotes H3K36me3 levels in mes-4 mutants. Our data thus identify OEF-1 as a novel modulator of the fundamental relationship between gene activation and gene silencing in the C. elegans germ line.
2020-03-24 | GSE147401 | GEO
Project description:A number of environmental factors (e.g. toxicants) have been shown to promote the epigenetic transgenerational inheritance of disease and phenotypic variation. Transgenerational inheritance requires the germline transmission of altered epigenetic information between generations in the absence of direct environmental exposures. The primary periods for epigenetic programming of the germline is associated with primordial germ cell development and during fetal gonadal sex determination. The current study examined the actions of an agricultural fungicide vinclozolin on gestating female (F0 generation) progeny in regards to the primordial germ cell (PGC) epigenetic reprogramming of the F3 generation (i.e. great-grandchildren). The F3 generation primordial germ cell transcriptome and epigenome (DNA methylation) was altered transgenerationally. Interestingly, the differential DNA methylation regions (DMR) and altered transcriptomes were distinct between the onset of gonadal sex determination at embryonic day 13 (E13) and after cord formation in the testis at embryonic day 16 (E16). A larger number of DMR and transcriptional alterations were observed in the E13 PGC than E16 germ cells. Observations demonstrate an altered transgenerational epigenetic reprogramming and function of the primordial germ cells and subsequent male germline is a component of vinclozolin induced epigenetic transgenerational inheritance of disease. Insights into the molecular control of germline transmitted epigenetic inheritance are provided. The combined observations demonstrate ancestral exposure of a gestating female during fetal gonadal sex determination can promote transgenerational alterations in the primordial germ cell and subsequent male germline epigenetic and transcriptional programming. This altered germline programming leads to the epigenetic transgenerational inheritance of disease and phenotypic variation. Observations support the role of the primordial germ cell programming in the molecular mechanism involved and provides insights into the molecular mechanisms that control the epigenetic transgenerational inheritance phenomena. Results suggest a cascade of epigenetic and transcriptional events during germ cell development is needed to obtain the mature germline epigenome that is then transmitted transgenerationally. RNA samples from PGC of 2 F3-control lineage groups were compared to PGC of 2 F3-vinclozolin lineage groups for two embryonic age E13 and E16
2013-01-17 | E-GEOD-43559 | biostudies-arrayexpress
Project description:In animals with germ plasm, specification of the germline involves “germ granules”, cytoplasmic condensates that enrich maternal transcripts in the germline founder cells. In C. elegans embryos, P granules enrich maternal transcripts, but surprisingly P granules are not essential for germ cell fate specification. Here we describe a second condensate in the C. elegans germ plasm. Like canonical P-bodies found in somatic cells, “germline P-bodies” contain regulators of mRNA decapping and deadenylation and, in addition, the intrinsically-disordered proteins MEG-1 and MEG-2 and the TIS11-family RNA-binding protein POS-1. Embryos lacking meg-1 and meg-2 do not stabilize P-body components, miss-regulate POS-1 targets, miss-specify the germline founder cell, and do not develop a germline. Our findings suggest that specification of the germ line involves at least two distinct condensates that independently enrich and regulate maternal mRNAs in the germline founder cells.
2022-10-04 | GSE211555 | GEO
Project description:A number of environmental factors (e.g. toxicants) have been shown to promote the epigenetic transgenerational inheritance of disease and phenotypic variation. Transgenerational inheritance requires the germline transmission of altered epigenetic information between generations in the absence of direct environmental exposures. The primary periods for epigenetic programming of the germline is associated with primordial germ cell development and during fetal gonadal sex determination. The current study examined the actions of an agricultural fungicide vinclozolin on gestating female (F0 generation) progeny in regards to the primordial germ cell (PGC) epigenetic reprogramming of the F3 generation (i.e. great-grandchildren). The F3 generation primordial germ cell transcriptome and epigenome (DNA methylation) was altered transgenerationally. Interestingly, the differential DNA methylation regions (DMR) and altered transcriptomes were distinct between the onset of gonadal sex determination at embryonic day 13 (E13) and after cord formation in the testis at embryonic day 16 (E16). A larger number of DMR and transcriptional alterations were observed in the E13 PGC than E16 germ cells. Observations demonstrate an altered transgenerational epigenetic reprogramming and function of the primordial germ cells and subsequent male germline is a component of vinclozolin induced epigenetic transgenerational inheritance of disease. Insights into the molecular control of germline transmitted epigenetic inheritance are provided. The combined observations demonstrate ancestral exposure of a gestating female during fetal gonadal sex determination can promote transgenerational alterations in the primordial germ cell and subsequent male germline epigenetic and transcriptional programming. This altered germline programming leads to the epigenetic transgenerational inheritance of disease and phenotypic variation. Observations support the role of the primordial germ cell programming in the molecular mechanism involved and provides insights into the molecular mechanisms that control the epigenetic transgenerational inheritance phenomena. Results suggest a cascade of epigenetic and transcriptional events during germ cell development is needed to obtain the mature germline epigenome that is then transmitted transgenerationally.
2013-01-17 | GSE43559 | GEO
Project description:A number of environmental factors (e.g. toxicants) have been shown to promote the epigenetic transgenerational inheritance of disease and phenotypic variation. Transgenerational inheritance requires the germline transmission of altered epigenetic information between generations in the absence of direct environmental exposures. The primary periods for epigenetic programming of the germ line are those associated with primordial germ cell development and subsequent fetal germline development. The current study examined the actions of an agricultural fungicide vinclozolin on gestating female (F0 generation) progeny in regards to the primordial germ cell (PGC) epigenetic reprogramming of the F3 generation (i.e. great-grandchildren). The F3 generation germline transcriptome and epigenome (DNA methylation) were altered transgenerationally. Interestingly, disruptions in DNA methylation patterns and altered transcriptomes were distinct between germ cells at the onset of gonadal sex determination at embryonic day 13 (E13) and after cord formation in the testis at embryonic day 16 (E16). A larger number of DNA methylation abnormalities (epimutations) and transcriptional alterations were observed in the E13 germ cells than in the E16 germ cells. These observations indicate that altered transgenerational epigenetic reprogramming and function of the male germline is a component of vinclozolin induced epigenetic transgenerational inheritance of disease. Insights into the molecular control of germline transmitted epigenetic inheritance are provided.
2014-07-17 | GSE59510 | GEO
Project description:A number of environmental factors (e.g. toxicants) have been shown to promote the epigenetic transgenerational inheritance of disease and phenotypic variation. Transgenerational inheritance requires the germline transmission of altered epigenetic information between generations in the absence of direct environmental exposures. The primary periods for epigenetic programming of the germ line are those associated with primordial germ cell development and subsequent fetal germline development. The current study examined the actions of an agricultural fungicide vinclozolin on gestating female (F0 generation) progeny in regards to the primordial germ cell (PGC) epigenetic reprogramming of the F3 generation (i.e. great-grandchildren). The F3 generation germline transcriptome and epigenome (DNA methylation) were altered transgenerationally. Interestingly, disruptions in DNA methylation patterns and altered transcriptomes were distinct between germ cells at the onset of gonadal sex determination at embryonic day 13 (E13) and after cord formation in the testis at embryonic day 16 (E16). A larger number of DNA methylation abnormalities (epimutations) and transcriptional alterations were observed in the E13 germ cells than in the E16 germ cells. These observations indicate that altered transgenerational epigenetic reprogramming and function of the male germline is a component of vinclozolin induced epigenetic transgenerational inheritance of disease. Insights into the molecular control of germline transmitted epigenetic inheritance are provided. The F0 generation females were exposed to a vehicle (dimethylsulfoxide DMSO) as control or to vinclozolin, as described in the Methods. The F1 generation offspring were bred to generate the F2 generation and the F2 generation offspring were bred to generate the F3 generation offspring. The timed pregnant F2 generation females were used to isolate the F3 generation control and vinclozolin lineage fetal gonads at the E13 and E16 time points. The F3 generation E13 PGC and E16 prospermatogonia were isolated. DNA was isolated from the freshly isolated cells to examine DNA methylation by methylated DNA immunoprecipitation (MeDIP) followed by analysis on a genome-wide promoter tiling array (Chip) using a comparative hybridization MeDIP-Chip analysis between control and vinclozolin lineage samples as described in Methods. This allowed a comparison of the epigenome alterations in F3 vinclozolin lineage germ cells at E13 and E16. Three separate experimental comparisons of control and vinclozolin-lineage animals involving different germ cell isolations were analyzed with three different MeDIP-Chip analyses at each time point.
2014-07-17 | E-GEOD-59510 | biostudies-arrayexpress
Project description:Germ granules are membrane-less organelles essential for small RNA biogenesis and germline development. Among the conserved properties of germ granules is their association with the nuclear membrane. Recent studies demonstrated that LOTUS domain proteins, EGGD-1 and EGGD-2 (also known as MIP-1 and MIP-2 respectively), promote the formation of perinuclear germ granules in C. elegans. This finding presents a unique opportunity to evaluate the significance of perinuclear localization of germ granules. Here we show that loss of eggd-1 causes the coalescence of germ granules and formation of abnormal cytoplasmic aggregates. Impairment of perinuclear granules affects certain germline classes of small RNAs including Piwi-interacting RNAs. Transcriptome profiling reveals overexpression of spermatogenic and cuticle-related genes in eggd-1 hermaphrodites. We further demonstrate that disruption of germ granules activates HLH-30-mediated transcriptional program in somatic tissues. Collectively, our findings underscore the essential role of EGGD-1 in germ granule organization and reveal an unexpected germ granule-to-soma communication.
2023-07-20 | GSE228857 | GEO