Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA385197 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5499062.fastq.gz | Fastqsanger.gz | |||
| SRR5499063.fastq.gz | Fastqsanger.gz | |||
| SRR5499064.fastq.gz | Fastqsanger.gz | |||
| SRR5499065.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
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Project description:Genome-wide Polycomb localization in Drosophila whole testes and purified germline precursor cells.
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Project description:Polycomb group gene E(z) is required for spermatogonial dedifferentiation in Drosophila adult testis
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Project description:In many metazoans, germ cells are separated from somatic lineages early in development and maintain their identity throughout life. Here we show that a Polycomb group (PcG) component, Enhancer of Zeste [E(z)] H3K27me3-specific methyltransferase, maintains germline identity in Drosophila adult testes. We find excessive early-stage somatic gonadal cells in E(z) mutant testes, which originate from both over-proliferative cyst stem cells and germ cells turning on an early-stage somatic cell marker. Using complementary lineage-tracing experiments in E(z) mutant testes, a portion of excessive early-stage somatic gonadal cells are found to derive from early-stage germ cells, including germline stem cells. Interestingly, knocking down E(z) specifically in somatic cells caused this germline-to-soma change, suggesting a non-cell autonomous role of E(z) to antagonize somatic identity in germ cells. Using fly testis specifically expressing E(z) shmiR RNAi in germ cells by nos promoter driven GAL4>UAS system, ChIPseq with H3K27me3 antibody was performed, where H3K27me3 is only detected in somatic cells.
2014-05-02 | E-GEOD-53238 | biostudies-arrayexpress
Project description:Drosophila whole testis gene expression
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Project description:Piwi is a key regulator of both somatic and germline stem cells in the Drosophila testis
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Project description:mRNA-sequencing data of Drosophila melanogaster testis
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Project description:Identification and annotation of all the genes in the sequenced Drosophila genome is a work in progress. Wild-type testis function requires many genes and is thus of potentially high value for the identification of transcription units. We therefore undertook a survey of the repertoire of genes expressed in the Drosophila testis by computational and microarray analysis. We generated 3141 high-quality testis expressed sequence tags (ESTs). Testis ESTs computationally collapsed into 1560 cDNA set used for further analysis. Of those, 11% correspond to named genes, and 33% provide biological evidence for a predicted gene. A surprising 47% fail to align with existing ESTs and 16% with predicted genes in the current genome release. EST frequency and microarray expression profiles indicate that the testis mRNA population is highly complex and shows an extended range of transcript abundance. Furthermore, >80% of the genes expressed in the testis showed onefold overexpression relative to ovaries, or gonadectomized flies. Additionally, >3% showed more than threefold overexpression at p <0.05. Surprisingly, 22% of the genes most highly overexpressed in testis match Drosophila genomic sequence, but not predicted genes. These data strongly support the idea that sequencing additional cDNA libraries from defined tissues, such as testis, will be important tools for refined annotation of the Drosophila genome. Additionally, these data suggest that the number of genes in Drosophila will significantly exceed the conservative estimate of 13,601. Keywords: other
2003-07-16 | GSE462 | GEO
Project description:The Drosophila spermatogenesis cell differentiation pathway involves the activation of a large set of genes in primary spermatocytes. Most of these genes are activated by testis-specific TATA-binding protein associated factors (tTAFs). In the current model for the activation mechanism, Polycomb plays a key role silencing these genes in the germline precursors, and tTAF-dependent activation in primary spermatocytes involves the displacement of Polycomb from gene promoters. We investigated the genome-wide binding of Polycomb in wild type and tTAF mutant testes. According to the model we expected to see a clear enhancement in Polycomb binding at tTAF-dependent spermatogenesis genes in tTAF mutant testes. However, we find little evidence for such an enhancement in tTAF mutant testes compared to wild type. To avoid problems arising from cellular heterogeneity in whole testis analysis, we further tested the model by analysing Polycomb binding in purified germline precursors, representing cells before tTAF-dependent gene activation. Although we find Polycomb associated with its canonical targets, we find little or no evidence of Polycomb at spermatogenesis genes. The lack of Polycomb at tTAF-dependent spermatogenesis genes in precursor cells argues against a model where Polycomb displacement is the mechanism of spermatogenesis gene activation.
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Project description:We conducted a genome-wide expression analysis of wild-type males using three cell populations isolated from mitotic, meiotic and post-meiotic phases of spermatogenesis in Drosophila melanogaster. Our approach was to directly isolate testis regions enriched with RNAs from each of the three specific germline phases. We used microarrays to detail the global gene expression profile in spermatogenesis and identified up- and down-regulated genes between two different spermatogenic phases in pairwise comparisons
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Project description:The Drosophila spermatogenesis cell differentiation pathway involves the activation of a large set of genes in primary spermatocytes. Most of these genes are activated by testis-specific TATA-binding protein associated factors (tTAFs). In the current model for the activation mechanism, Polycomb plays a key role silencing these genes in the germline precursors, and tTAF-dependent activation in primary spermatocytes involves the displacement of Polycomb from gene promoters. We investigated the genome-wide binding of Polycomb in wild type and tTAF mutant testes. According to the model we expected to see a clear enhancement in Polycomb binding at tTAF-dependent spermatogenesis genes in tTAF mutant testes. However, we find little evidence for such an enhancement in tTAF mutant testes compared to wild type. To avoid problems arising from cellular heterogeneity in whole testis analysis, we further tested the model by analysing Polycomb binding in purified germline precursors, representing cells before tTAF-dependent gene activation. Although we find Polycomb associated with its canonical targets, we find little or no evidence of Polycomb at spermatogenesis genes. The lack of Polycomb at tTAF-dependent spermatogenesis genes in precursor cells argues against a model where Polycomb displacement is the mechanism of spermatogenesis gene activation. This genome-wide ChIP-array study investigates the binding of Polycomb in three biological samples: wild type (WT) whole testes, tTAF (can) mutant whole testes, and FACS-sorted germline precursor cells. We performed two biological replicates for each sample, except wild type whole testes where we performed three. For all ChIP-array experiments, input chromatin was used as the reference control to assay ChIP enrichment. We used Cy3/Cy5-labelled ChIP and input DNA for hybridisation onto Nimblegen arrays, and we performed a Cy3/Cy5 dye swap for one biological replicate of each sample (see supplementary file: GSE39935_README.txt).
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