Genome-wide study of the role of the histone demethylase dLsd1 in oogenesis
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE110751 | GEO | 2019/11/21
REPOSITORIES: GEO
Similar Datasets
Project description:The histone demethylase LSD1 is a key chromatin regulator that plays a crucial role in development. It has been shown to act both as a co-repressor and a co-activator of genes expression and to affect the expression of many genes important for development. In Drosophila, dLsd1 is essential for oogenesis; however, our current knowledge of dLsd1 function is insufficient to explain its precise role in the ovary. To better define the role of dLsd1 in oogenesis, we performed genome-wide analysis of dLsd1 binding in the ovary by Chromatin Immunoprecipitation followed by sequencing (ChIP-Seq).
2019-02-08 | GSE110331 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE17333: Oogenesis in Solea senegalensis: Vitellogenic versus mature ovaries GSE17334: Oogenesis in Solea senegalensis: vitellogenic versus atretic ovaries GSE17335: Oogenesis in Solea senegalensis: mature versus atretic ovaries GSE17336: Oogenesis in Solea senegalensis: Previtellogenic versus vitellogenic ovaries Refer to individual Series
2010-06-21 | E-GEOD-17337 | biostudies-arrayexpress
Project description:Genome-wide study of the role of the histone demethylase dLsd1 in oogenesis
| PRJNA433482 | ENA
Project description:Genome-wide study of the role of the histone demethylase dLsd1 in oogenesis
| PRJNA434461 | ENA
Project description:Nutrient-responsive oogenesis in Drosophila is a complex and dynamic process regulated, in part, by members of the Pc and Trx complexes. The recent finding that O-GlcNAc Transferase (ogt/sxc) is essential for Pc repression raises the question of whether this nutrient-sensing pathway plays a role in regulating oogenesis. OGT transfers O-GlcNAc to key transcriptional regulators in response to graded levels of the nutrient-derived precursor UDP-GlcNAc; O-GlcNAcase (OGA) catalyzes the removal of O-GlcNAc. Here we produced a null allele of oga (oga1) in Drosophila to examine its in vivo function. We found that oga mutant flies were viable, but that females displayed greatly reduced fecundity. The ovaries from the female OGA knockout exhibited a starvation-like phenotype, even under well-fed conditions. Germline stem cell division was slowed in the germarium of OGA knockout fly ovarioles. Ovaries from the oga1 mutants displayed significantly decreased H3K4 monomethylation in germline stem cells. The Trithorax family members Trx and Ash1 and Compass member Set1 histone methyltransferases are O-GlcNAc modified in oga1 mutant ovaries. Our results suggest that the loss of OGA disrupts oogenesis at least in part by interfering with H3K4 monomethylation in germ cells in the ovary. The findings also suggest that O-GlcNAc cycling is an essential part of the nutrient-responsive epigenetic machinery regulating Drosophila oogenesis in response to a changing nutrient supply.
2017-01-09 | GSE65197 | GEO
Project description:During Drosophila oogenesis, the localization and translational regulation of maternal transcripts relies on RNA-binding proteins (RBPs). Many of these RBPs localize several mRNAs and may have additional direct interaction partners to regulate their functions. Using immunoprecipitation from whole Drosophila ovaries coupled to mass spectrometry, we examined protein-protein associations of 6 GFP-tagged RBPs expressed at physiological levels. Analysis of the interaction network and further validation in human cells allowed us to identify 26 previously unknown associations, besides recovering several well characterized interactions.
2020-06-22 | PXD016680 | Pride
Project description:Increasing evidence indicates that ribosomes are heterogeneous and perhaps dynamic, in contrast to the classical view of them as constitutive machinery for protein synthesis [1-11]. In Drosophila melanogaster, nine ribosomal protein genes are each present in two paralogs, and in many of these cases one of the paralogs is primarily expressed in germline tissues [12-14]. Among these are two genes encoding ribosomal protein S5, called RpS5a and RpS5b. We demonstrate that RpS5b is specifically required for oogenesis. Females lacking RpS5b produce ovaries with polarity defects, fused egg chambers, and over-proliferation of posterior follicle cells. Oogenesis ceases at stage 8-9, and widespread apoptosis follows. Females lacking germline RpS5a are fully fertile, but germline expression of interfering RNA targeting RpS5a in an RpS5b mutant background worsens the RpS5b phenotype and causes complete germline lethality. A broad spectrum of mRNAs co-purified in immunoprecipitations with RpS5a, while RpS5b-associated mRNAs were specifically enriched for GO terms related to mitochondrial electron transport and cellular metabolic processes. Consistent with this, proteome comparison of wildtype and RpS5b ovaries revealed that RpS5b mitochondria were depleted for proteins linked to oxidative phosphorylation and mitochondrial respiration. As observed by immunohistochemical staining and transmission electron microscopy, RpS5b nurse cell mitochondria tended to form large clusters and had more heterogeneous morphology than those from controls. We also observed that RpS5b ovaries have elevated ROS, consistent with mitochondrial dysfunction. We conclude that RpS5b-containing ribosomes preferentially associate with mRNAs encoding mitochondrial components and serve an essential function in oogenesis.
2018-10-20 | GSE121533 | GEO
Project description:Global transcriptome analysis identifies regulated transcripts and pathways activated during oogenesis and early embryogenesis in Atlantic cod
2014-02-01 | E-MTAB-2170 | biostudies-arrayexpress
Project description:EHMT1 (also known as GLP) is a multifunctional protein, best known for its role as an H3K9me1 and H3K9me2 methyltransferase through its reportedly obligatory dimerization with EHMT2 (also known as G9A). Here, we investigated the role of EHMT1 in the oocyte in comparison to EHMT2 using oocyte-specific conditional knockout mouse models (Ehmt2 cKO, Ehmt1cKO, Ehmt1/2 cDKO), with ablation from the early phase of oocyte growth. Loss of EHMT1 in Ehmt1 cKO and Ehmt1/2 cDKO oocytes recapitulated meiotic defects observed in the Ehmt2 cKO; however, there was a significant impairment in oocyte maturation and developmental competence in Ehmt1 cKO and Ehmt1/2 cDKO oocytes beyond that observed in the Ehmt2cKO. Consequently, loss of EHMT1 in oogenesis results, upon fertilization, in mid-gestation embryonic lethality. To identify H3K9 methylation and other meaningful biological changes in each mutant to explore the molecular functions of EHMT1 and EHMT2, we performed immunofluorescence imaging, multi-omics sequencing, and mass spectrometry (MS)–based proteome analyses in cKO oocytes. Although H3K9me1 was depleted only upon loss of EHMT1, H3K9me2 was decreased, and H3K9me2-enriched domains were eliminated equally upon loss of EHMT1 or EHMT2. Furthermore, there were more significant changes in the transcriptome, DNA methylome, and proteome in Ehmt1/2 cDKO than Ehmt2 cKO oocytes, withtranscriptional derepression leading to increased protein abundance and local changes in genic DNA methylation in Ehmt1/2 cDKO oocytes. Together, our findings suggest that EHMT1 contributes to local transcriptional repression in the oocyte, partially independent of EHMT2, and is critical for oogenesis and oocyte developmental competence
2023-01-30 | PXD030265 | Pride
Project description:Argonaute2 proteins (Ago2) are key component of RNA-induced gene silencing complexes (RISCs), which is crucial for microRNAs to repress target genes. The function of Ago2 for oogenesis is unknown due to early embryonic lethal of Ago2 knockout mice. Here we show the effect of loss of Ago2 in mouse oogenesis by specific deletion of it in growing oocyte. Although the Ago2-deficient oocytes can develop to mature oocytes, they have abnormal spindle and the chromosomes that can’t cluster together properly, which are very similar to the phenotype of Dicer-deficient oocytes. We checked miRNA expression profile and found that in Ago2-deficient oocyte, the expression of most miRNAs reduced more than 80%. To understand the downstream genes regulated by Ago2, we used microarray on Ago2-deficient oocyte and found that 512 genes were upregulated and 1073 genes were downregulated (FC>2, P<0.05). Our data proved that Ago2 have a key function for mouse oogenesis through globally regulating miRNA stability and function.
2009-09-01 | GSE15529 | GEO