Piwi mutations and c-Fos overexpression on Drosophila ovarian germline
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE69722 | GEO | 2017/02/08
SECONDARY ACCESSION(S): PRJNA286259
REPOSITORIES: GEO
Similar Datasets
Project description:Drosophila melanogaster Piwi functions within the germline stem cells (GSCs) and the somatic niche to regulate GSC self-renewal and differentiation. How Piwi influences GSCs is largely unknown. We uncovered a genetic interaction between Piwi and c-Fos in the somatic niche that influences GSCs. c-Fos is a proto-oncogene that influences many cell and developmental processes. In wild-type ovarian cells, c-Fos is post-transcriptionally repressed by Piwi, which destabilized the c-Fos mRNA by promoting the processing of its 3' untranslated region (UTR) into Piwi-interacting RNAs (piRNAs). The c-Fos 3' UTR was sufficient to trigger Piwi-dependent destabilization of a GFP reporter. Piwi represses c-Fos in the somatic niche to regulate GSC maintenance and differentiation and in the somatic follicle cells to affect somatic cell disorganization, tissue dysmorphogenesis, oocyte maturation arrest, and infertility.
| S-EPMC5021354 | biostudies-literature
Project description:Piwi regulates niche and intrinsic mechanisms to maintain germline stem cells in Drosophila, yet how this regulation occurs remains elusive. Here, we show that Piwi interacts with the Polycomb Group Complexes PRC1 and PRC2 to maintain ovarian germline stem cells and oogenesis, as well as to repress retrotransposons. Piwi binds to PRC2 subunits Su(z)12 and Esc in vitro and forms a complex with PRC2 in vivo. Whole-genome analyses of PRC2-mediated histone 3 lysine 27 trimethylation (H3K27m3) in wild type and piwi mutant ovarian nuclei indicate that Piwi inhibits H3K27m3 at PRC2 target genes that are mostly regulators of development and transcription.
2017-01-03 | GSE40150 | GEO
Project description:piRNAs function in silencing retrotransposons by associating with the PIWI proteins, AGO3, Aub, and Piwi, in Drosophila germlines. Bioinformatics analyses of piRNAs in Drosophila ovaries suggested that piRNAs are produced by two systems, the primary processing pathway and the amplification loop, from repetitive genes and piRNA clusters in the genome. The amplification loop occurs in a Dicer-independent, PIWI-Slicer-dependent manner. However, the primary processing pathway remains largely conceptual. Here we show that in ovarian somatic cells, which lack Aub and AGO3 but express Piwi, the primary processing pathway for piRNAs indeed exists. Keywords: Small RNA profiling by high throughput sequencing Piwi-associated small RNAs were extracted from Drosophila ovarian somatic cells and their deep sequencing was carried out.
2009-10-01 | E-GEOD-15137 | biostudies-arrayexpress
Project description:piRNAs function in silencing retrotransposons by associating with the PIWI proteins, AGO3, Aub, and Piwi, in Drosophila germlines. Bioinformatics analyses of piRNAs in Drosophila ovaries suggested that piRNAs are produced by two systems, the primary processing pathway and the amplification loop, from repetitive genes and piRNA clusters in the genome. The amplification loop occurs in a Dicer-independent, PIWI-Slicer-dependent manner. However, the primary processing pathway remains largely conceptual. Here we show that in ovarian somatic cells, which lack Aub and AGO3 but express Piwi, the primary processing pathway for piRNAs indeed exists. Keywords: Small RNA profiling by high throughput sequencing
2009-10-02 | GSE15137 | GEO
Project description:Analysis of Piwi-piRNAs that assocaite with wild type Piwi and specificity loop (SL) mutants in ovarian somatic sheath cells (OSC) and Droosphila ovaries.
2019-01-30 | GSE115839 | GEO
Project description:Background: Endometrialcyst of ovary (EMC) may develop into endometriosis-associated ovarian cancer over time (EAOC). EAOC pathogenesis is unknown. This study investigated the likely mechanism of EAOC publishing related with orthotopic endometrial, searched for a feasible biomarker using RNA sequencing, and examined the molecular function of this biomarker in ectopic endometrial cells from EAOC and EMC patients. Methods: RNA sequencing was performed on 5 EAOC and 4 EMC tissue samples. Differential expression analysis employed RNA-seq data. To identify biomarkers, differential genes were used in PPI network design, GO pathway enrichment, and GSEA pathway enrichment. Immunohistochemical staining revealed FOS expression in various endometrium. Lv-FOS was utilized to up-regulate FOS in hEnSCs, and cell counting kit-8 (CCK-8), colony formation assay, and scratch assay were performed to assess cell viability, proliferation, and migration. Western blot showed protein expression alterations. Results: 249 genes were differently expressed, including FOS. Pathway enrichment study demonstrated that MAPK, AP-1, ERK, and other signaling pathways were involved in EMC-to-EAOC conversion. FOS upregulation in hEnSCs increased cell viability, proliferation, and migration. Western blot results showed that FOS, CDK4, cyclinD1, P21, and invasion-related proteins p-stat3, MMP2, and MMP9 were up- or down-regulated, respectively. Conclusion: Mitosis and cell cycle affect EMC to EAOC progression. FOS expression, a novel biomarker, promotes EMC transition into EAOC and endometrial cell proliferation, invasion, and migration. Keywords: FOS, endometrialcyst of ovary, endometriosis-associated ovarian cancer, biomarker
2023-05-23 | GSE226575 | GEO
Project description:Insertions of transposable elements (TEs) in eukaryotic genomes are usually associated with repressive chromatin, which spreads to neighbouring genomic sequences. In ovaries of Drosophila melanogaster, the Piwi-piRNA pathway plays a key role in the transcriptional silencing of TEs considered to be exerted mostly through the establishment of H3K9me3 histone marks recruiting Heterochromatin Protein 1a (HP1a). Here, using RNA-seq, we investigated the expression of TEs and the adjacent genomic regions upon Piwi and HP1a germline knockdowns sharing a similar genetic background. We found that the depletion of Piwi and HP1a led to the derepression of only partially overlapping TE sets. Several TEs were silenced predominantly by HP1a, whereas the upregulation of some other TEs was more pronounced upon Piwi knockdown and, surprisingly, was diminished upon a Piwi/HP1a double-knockdown. We revealed that HP1a loss influenced the expression of thousands of protein-coding genes mostly not adjacent to TE insertions and, in particular, downregulated a putative transcriptional factor required for TE activation. Nevertheless, our results indicate that Piwi and HP1a cooperatively exert repressive effects on the transcription of euchromatic loci flanking the insertions of some Piwi-regulated TEs. We suggest that this mechanism controls the silencing of a small set of TE-adjacent tissue-specific genes, preventing their inappropriate expression in ovaries.
2021-12-22 | GSE186867 | GEO
Project description:Drosophila Piwi associates with PIWI-interacting RNAs (piRNAs) and represses transposons transcriptionally through heterochromatinization; however, this process is poorly understood. Here, we identify Brahma (Brm), the core adenosine triphosphatase of the SWI/SNF chromatin remodeling complex, as a new Piwi interactor, and show Brm involvement in activating transcription of Piwi-targeted transposons before silencing. Bioinformatic analyses indicated that Piwi, once bound to target RNAs, reduced the occupancies of SWI/SNF and RNA polymerase II (Pol II) on target loci, abrogating transcription. Artificial piRNA-driven targeting of Piwi to RNA transcripts enhanced repression of Brm-dependent reporters compared with Brm-independent reporters. This was dependent on Piwi cofactors, Gtsf1/Asterix (Gtsf1), Panoramix/Silencio (Panx), and Maelstrom (Mael), but not Eggless/dSetdb (Egg)–mediated H3K9me3 deposition. The lambdaN-box B–mediated tethering of Mael to reporters repressed Brm-dependent genes in the absence of Piwi, Panx, and Gtsf1. We propose that Piwi, via Mael, can rapidly suppress transcription of Brm-dependent genes to facilitate heterochromatin formation.
2020-12-13 | GSE108329 | GEO
Project description:The Piwi-piRNA pathway is well known for its germline function, yet its somatic role remains elusive. We show here that Piwi is required autonomously not only for germline stem cell (GSC) but also for somatic cyst stem cell (CySC) maintenance in the Drosophila testis. Reducing Piwi activity in the testis caused defects in CySC differentiation. Accompanying this, GSC daughters expanded beyond the vicinity of the hub but failed to differentiate further. Moreover, Piwi deficient in nuclear localization caused similar defects in somatic and germ cell differentiation, which was rescued by somatic Piwi expression. To explore the underlying molecular mechanism, we identified Piwi-bound piRNAs that uniquely map to a gene key for gonadal development, Fasciclin 3, and demonstrate that Piwi regulates its expression in somatic cyst cells. Our work reveals the cell-autonomous function of Piwi in both somatic and germline stem cell types, with somatic function possibly via its epigenetic mechanism. Examination of Piwi-piRNAs in fly testis
2015-05-23 | E-GEOD-68997 | biostudies-arrayexpress
Project description:The Piwi-piRNA pathway is well known for its germline function, yet its somatic role remains elusive. We show here that Piwi is required autonomously not only for germline stem cell (GSC) but also for somatic cyst stem cell (CySC) maintenance in the Drosophila testis. Reducing Piwi activity in the testis caused defects in CySC differentiation. Accompanying this, GSC daughters expanded beyond the vicinity of the hub but failed to differentiate further. Moreover, Piwi deficient in nuclear localization caused similar defects in somatic and germ cell differentiation, which was rescued by somatic Piwi expression. To explore the underlying molecular mechanism, we identified Piwi-bound piRNAs that uniquely map to a gene key for gonadal development, Fasciclin 3, and demonstrate that Piwi regulates its expression in somatic cyst cells. Our work reveals the cell-autonomous function of Piwi in both somatic and germline stem cell types, with somatic function possibly via its epigenetic mechanism.
2015-05-23 | GSE68997 | GEO