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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The effect of HP1-gamma deficiency on primordial germ cells

ABSTRACT: We compared the gene expression profiles of the HP1 gamma -/- vs wild-type PGCs to examine the molecular mechanisms of HP1g in PGC development. Although HP1g is suggested to be involved in PGC proliferation, our microarray data indicated that HP1g does not directly control PGC cell-cycle progression by regulating cell cycle-related genes. However, many genes acting on differentiated tissues were up-regulated in the HP1g-/- PGCs. The mVenus-positive cells from the E11.5 genital ridges were isolated by flow cytometry (JSAN, Bay Bioscience). The total RNA was then prepared from the sorted primordial germ cells (about 500-3,500 cells per embryo) of wild-type or HP1?-/- embryos with an RNeasy micro kit (Qiagen). The RNA samples were pooled from 5 or 6 embryos of each genotype. Two independent pooled RNA samples of each genotypes were used to verify the reproducibility of the microarray analyses.

ORGANISM(S): Mus musculus

SUBMITTER: Masahide Asano

PROVIDER: E-GEOD-27294 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Loss of heterochromatin protein 1 gamma reduces the number of primordial germ cells via impaired cell cycle progression in mice.

Abe Kanae K Naruse Chie C Kato Tomoaki T Nishiuchi Takumi T Saitou Mitinori M Asano Masahide M

Biology of reproduction 20110720 5

Signals from extraembryonic tissues in mice determine which proximal epiblast cells become primordial germ cells (PGCs). After their specification, approximately 40 PGCs appear at the base of the allantoic bud and migrate to the genital ridges, where they expand to about 25 000 cells by Embryonic Day (E)13.5. The heterochromatin protein 1 (HP1) family members HP1alpha, HP1beta, and HP1gamma (CBX5, CBX1, and CBX3, respectively) are thought to induce heterochromatin structure and to regulate gene ...[more]

PMID: 21778144

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The effect of HP1-gamma deficiency on primordial germ cells

Project description:We compared the gene expression profiles of the HP1 gamma -/- vs wild-type PGCs to examine the molecular mechanisms of HP1g in PGC development. Although HP1g is suggested to be involved in PGC proliferation, our microarray data indicated that HP1g does not directly control PGC cell-cycle progression by regulating cell cycle-related genes. However, many genes acting on differentiated tissues were up-regulated in the HP1g-/- PGCs.

2011-08-01 | GSE27294 | GEO

Role of Ror2 in primordial germ cell migration

Project description:Primordial germ cells (PGCs), the embryonic precursors of eggs and sperm, are a unique model for identifying and studying regulatory mechanisms in singly migrating cells. From their time of specification to eventual colonization of the gonad, mouse PGCs traverse through and interact with many different cell types, including epithelial cells and mesenchymal tissues. Work in drosophila and zebrafish have identified many genes and signaling pathways involved in PGC migration, but little is known about this process in mammals. We have generated a point mutation in the Ror2 gene that we know disrupts primordial germ cell migration in the developing mouse embryo. We used microarray analysis to determine if this defect is mediated through genome-wide or pathway-specific transcriptional changes. We analyzed primordial germ cells (PGCs) from 4 wild-type (WT) and 4 Ror2Y324C/Y324C mutant embryos using Oct4-DPE-EGFP. PGCs were collected during their active migratory state at embryonic day 9.5 (somite range 20-25).

2014-08-08 | E-GEOD-60179 | biostudies-arrayexpress

PRC1 coordinates timing of sexual differentiation of female primordial germ cells

Project description:In mammals, sex differentiation of primordial germ cells (PGCs) is determined by extrinsic cues from the environment1. In female PGCs, expression of Stimulated by retinoic acid 8 (Stra8) and meiosis are induced in response to retinoic acid (RA) provided by the mesonephroi2-4. Given the widespread role of RA signaling during development8,9, the molecular mechanism specifying the competence of PGCs to timely express Stra8 and enter meiosis are unknown2,10. Here we identify gene dosage dependent roles in PGC development for Ring1 and Rnf2, two central components of the Polycomb Repressive Complex 1 (PRC1)11,13. Both paralogs are essential for PGC development between day 10.5 and 11.5 of gestation. Rnf2 is subsequently required in female PGCs for maintaining high levels of Oct4 and Nanog expression6, and for preventing premature induction of meiotic gene expression and entry into meiotic prophase. Chemical inhibition of RA signaling partially suppresses precocious Oct4 down-regulation and Stra8 activation in Rnf2-deficient female PGCs. Chromatin immunoprecipitation analyses show that Stra8 is a direct target of PRC1 and PRC2 in PGCs. These data demonstrate the importance of PRC1 gene dosage in PGC development and in coordinating the timing of sex differentiation of female PGCs by antagonizing extrinsic RA signaling. Gene expression of mouse primordial germ cells was analysed using Affymetrix microarray. Primodial germ cells were purified from embryos carrying Oct4(deltaPE)-GFP transgene by FACS.

2013-03-14 | E-GEOD-42782 | biostudies-arrayexpress

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2014-08-01 | E-GEOD-48897 | biostudies-arrayexpress

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Project description:Genome-wide DNA demethylation, including the erasure of genome imprints, in primordial germ cells (PGCs), is critical as a first step for creating the totipotent epigenome in the germ line. Here, we provide evidence that contrary to the prevailing model involving active DNA demethylation, imprint erasure in mouse PGCs occurs in a manner consistent with replication-coupled passive DNA demethylation: PGCs erase imprints during their rapid proliferation with little de novo as well as maintenance DNA methylation potential and no major chromatin alterations. Our findings necessitate the re-evaluation of and provide novel insights into the mechanism of genome-wide DNA demethylation in PGCs. We performed expression analysis of primordial germ cells (PGCs) at embryonic days 10.5-13.5. Because the number of PGCs available at these stages were low, cDNAs were amplified by the method that we previously published (Kurimoto et al. 2006, NAR 34: e42 (PMID 16547197)). To include analysis of PGC gene expression at E9.5, we re-normalized the data from our E9.5 PGC samples (GSM744103, GSM744104) from our previous publication (Hayashi et al., 2011, Cell 146: 519-32 (PMD 21820164)) together with the data from this submission.

2013-03-04 | E-GEOD-40412 | biostudies-arrayexpress

The Xenopus Primordial Germ Cell Transcriptome: Unexpected Role for sox7 in Early PGC Development

Project description:Xenopus primordial germ cells (PGCs) are determined by the presence of maternally derived germ plasm. Germ plasm components both protect PGCs from somatic differentiation and begin a unique gene expression program. Segregation of the germline from the endodermal lineage occurs during gastrulation and PGCs subsequently initiate zygotic transcription. However, the gene-networks that operate to both preserve the potential for totipotency and promote germline differentiation are poorly understood. Here, we utilized RNA-sequencing analysis to comprehensively interrogate PGC and neighboring endoderm cell RNAs after lineage segregation. We identified 1,865 transcripts enriched in PGCs compared to endoderm cells. Over 50% of maternal, vegetally-enriched transcripts were enriched in the PGC transcriptome, including sox7. PGC-directed sox7 knockdown and over-expression studies revealed an early requirement for sox7 in proper germ plasm localization, zygotic transcription, and PGC number. We identified oct60 as the most highly expressed and enriched OCT3/4 homologue in PGCs. Lastly, we compared the Xenopus PGC transcriptome with human PGC transcripts and showed that 80% of transcripts are conserved, identifying Xenopus as a relevant model system for understanding the gene-networks necessary for human germline development.

2017-08-01 | GSE102047 | GEO

Max is a repressor of germ-cell-related gene expression in mouse embryonic stem cells

Project description:Embryonic stem cells (ESCs) and primordial germ cells (PGCs) express many pluripotency-associated genes, but ESCs do not normally undergo conversion into PGCs. Thus, we predicted that there is a mechanism that represses PGC-related gene expression in ESCs. Here we identify genes involved in this putative mechanism, by using an ESC line with a Vasa reporter for an RNAi screen of transcription factor genes expressed in ESCs. We identify 5 genes that result in the expression of Vasa when silenced. Of these, Max is the most striking. Transcriptome analysis reveals that Max knockdown (KD) in ESCs results in selective, global derepression of germ-cell-specific genes. Max interacts with histone H3K9 methyltransferases and associates with the germ-cell-specific genes in ESCs. In addition, Max-KD results in a decrease in histone H3K9 dimethylation at their promoter regions. We propose that Max is part of a protein complex that acts as a repressor of germ-cell-related genes in ESCs. Gene expression profile of Vasa-positive cells isolated from Max knockdown ESCs was compared to that of normal ESCs and in vivo PGCs. As an ESCs sample, a mouse embryonic stem cell line that carries a Venus reporter driven by the Vasa gene promoter (VV3) was used for this study. VV3 ESCs were transfected with non-silencing negative control siRNA (AllStars) or siRNA against the Max gene. Vasa-positive cells were purified using fluorescence-activated cell sorting (FACS). As a PGCs sample, a mouse strain that carries a germ-cell-specific GFP reporter (Oct4M-NM-^TPE-GFP) was used. PGCs were also purified using FACS. RNA samples were isolated from each sample and labeled and hybridized to Agilent microarrays. Three biological replicates were performed for each group of samples.

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The Heterochromatin protein 1 is a master regulator in RNA splicing precision deficient in ulcerative colitis

Project description:Defects in RNA splicing have been linked to numerous human disorders, but remain poorly explored in inflammatory bowel disease (IBD). Here, we report that, in the gut epithelium of patients with ulcerative colitis (UC), the expression of the chromatin and alternative splicing regulator HP1g is strongly reduced. Accordingly, inactivation of the HP1g gene in the mouse gut triggered several IBD-like traits, including inflammation and dysbiosis. In parallel, we discovered that its loss of function broadly increased splicing noise, reducing requirement for canonical splicing consensus sequences, and favoring the usage of cryptic splice sites at numerous genes with key functions in gut biology. This notably resulted in the production of progerin, a noncanonical toxic splice variant of prelamin A mRNA, responsible for the Hutchinson Gilford Progeria Syndrome (HGPS) of premature aging. Likewise, production of progerin transcript was found to be a signature of colonic cells from UC patients. Thus, our study identifies HP1g as a regulator of RNA metabolism in vivo, providing a unique mechanism linking anti-inflammation and accuracy of RNA splicing in the gut epithelium. HP1 defect may confer a general disturbance in RNA splicing precision to scrutinize in IBD and more generally in accelerating aging diseases.

2022-10-25 | PXD031580 | Pride

PRC1 coordinates timing of sexual differentiation of female primordial germ cells (RNA-Seq)

Project description:In mammals, sex differentiation of primordial germ cells (PGCs) is determined by extrinsic cues from the environment1. In female PGCs, expression of Stimulated by retinoic acid 8 (Stra8) and meiosis are induced in response to retinoic acid (RA) provided by the mesonephroi2-4. Given the widespread role of RA signaling during development8,9, the molecular mechanism specifying the competence of PGCs to timely express Stra8 and enter meiosis are unknown2,10. Here we identify gene dosage dependent roles in PGC development for Ring1 and Rnf2, two central components of the Polycomb Repressive Complex 1 (PRC1)11,13. Both paralogs are essential for PGC development between day 10.5 and 11.5 of gestation. Rnf2 is subsequently required in female PGCs for maintaining high levels of Oct4 and Nanog expression6, and for preventing premature induction of meiotic gene expression and entry into meiotic prophase. Chemical inhibition of RA signaling partially suppresses precocious Oct4 down-regulation and Stra8 activation in Rnf2-deficient female PGCs. Chromatin immunoprecipitation analyses show that Stra8 is a direct target of PRC1 and PRC2 in PGCs. These data demonstrate the importance of PRC1 gene dosage in PGC development and in coordinating the timing of sex differentiation of female PGCs by antagonizing extrinsic RA signaling. Gene expression of mouse primordial germ cells was analysed using RNAseq method. Primodial germ cells were purified from embryos carrying Oct4(-delta-PE)-GFP transgene by FACS.

2013-03-14 | E-GEOD-42852 | biostudies-arrayexpress

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