Transcriptional factor Tj is the master regulator of the somatic piRNA pathway in the Drosophila ovarian follicle cells [smallRNA-seq]
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ABSTRACT:
PROVIDER: PRJNA1186703 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31362777.fastq.gz | Fastqsanger.gz | |||
| SRR31362778.fastq.gz | Fastqsanger.gz | |||
| SRR31362779.fastq.gz | Fastqsanger.gz | |||
| SRR31362780.fastq.gz | Fastqsanger.gz | |||
| SRR31362781.fastq.gz | Fastqsanger.gz |
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Project description:Transposable elements (TEs) pose a threat to genome integrity, and the piRNA pathway in animal gonads plays a crucial role in silencing TE activity. While the transcriptional regulation of piRNA pathway components in germline cells is well understood, the mechanisms orchestrating the transcriptional program of the somatic piRNA pathway in surrounding somatic cells remains poorly defined. Here, we demonstrate that Traffic Jam (Tj), an orthologue of a large Maf transcription factor in mammals, is a master regulator of the somatic piRNA pathway playing a crucial role in maintaining TE silencing and genomic integrity in somatic tissues . We show that Tj directly binds to the promoters of piRNA factors such as fs(1)Yb, nxf2, panx, and armi, as well as the flamenco piRNA cluster, a major locus for TE silencing in somatic cells. Knockdown of Tj in somatic follicle cells results in significant downregulation of these piRNA factors, a complete loss of flam expression, and derepression of TEs. We have identified an enhancer downstream of the flam promoter, including TJ binding sites, essential for high and specific flam expression in ovarian follicle cells in adult ovaries. This work uncovers a previously unappreciated layer of transcriptional regulation oc the piRNA pathway and we propose that Tj evolved to orchestrate the somatic piRNA pathway expression, ensuring efficient TE silencing in somatic cells that support germ cells, thereby preventing instability from being transmitted to the offspring.
2025-04-11 | GSE282039 | GEO
Project description:Transposable elements (TEs) pose a threat to genome integrity, and the piRNA pathway in animal gonads plays a crucial role in silencing TE activity. While the transcriptional regulation of piRNA pathway components in germline cells is well understood, the mechanisms orchestrating the transcriptional program of the somatic piRNA pathway in surrounding somatic cells remains poorly defined. Here, we demonstrate that Traffic Jam (Tj), an orthologue of a large Maf transcription factor in mammals, is a master regulator of the somatic piRNA pathway playing a crucial role in maintaining TE silencing and genomic integrity in somatic tissues . We show that Tj directly binds to the promoters of piRNA factors such as fs(1)Yb, nxf2, panx, and armi, as well as the flamenco piRNA cluster, a major locus for TE silencing in somatic cells. Knockdown of Tj in somatic follicle cells results in significant downregulation of these piRNA factors, a complete loss of flam expression, and derepression of TEs. We have identified an enhancer downstream of the flam promoter, including TJ binding sites, essential for high and specific flam expression in ovarian follicle cells in adult ovaries. This work uncovers a previously unappreciated layer of transcriptional regulation oc the piRNA pathway and we propose that Tj evolved to orchestrate the somatic piRNA pathway expression, ensuring efficient TE silencing in somatic cells that support germ cells, thereby preventing instability from being transmitted to the offspring.
2025-04-11 | GSE275646 | GEO
Project description:Transcriptional factor Tj is the master regulator of the somatic piRNA pathway in the Drosophila ovarian follicle cells
| PRJNA1186699 | ENA
Project description:Transcriptional factor Tj is the master regulator of the somatic piRNA pathway in the Drosophila ovarian follicle cells [RNA-seq]
| PRJNA1152487 | ENA
Project description:The PIWI-interacting RNA (piRNA) pathway is essential for transposable element (TE) silencing in animal gonads. While the transcriptional regulation of piRNA pathway components in germ cells has been documented in mice and flies, their control in somatic cells of Drosophila ovaries remains unresolved. Here, we demonstrate that Traffic jam (Tj), the Drosophila orthologue of large Maf transcription factors in mammals, is a master regulator of the somatic piRNA pathway. Tj binds to regulatory regions of somatic piRNA factors and the major piRNA cluster flamenco, which carries a Tj-bound enhancer downstream of its promoter. Depletion of Tj in somatic follicle cells causes downregulation of piRNA factors, loss of flam expression and de-repression of gypsy-family TEs. We propose that the arms race between the host and TEs led to the co-evolution of promoters in piRNA pathway genes as well as TE regulatory regions that both rely on a shared transcription factor.
2026-01-23 | GSE287891 | GEO
Project description:The flamenco (flam) locus is the most prominent piRNA cluster locus expressed in Drosophila ovarian follicle cells that is required for female fertility and silencing of gypsy/mdg4 transposons. Although P-element insertions in the flam promoter region disrupts flam piRNAs and cause female infertility, the flam enhancer architecture is still poorly understood. To illuminate flam’s regulation, we uncovered novel shadow enhancer (SE) sequences within the first exons of flam via promoter-bashing assays in OSS cells. We confirmed the SE relevance in vivo with new Drosophila flam deletion mutants of these regions that compromised flam piRNA expression and lowered female fertility from unleashed transposon expression. In a proteomic analysis of proteins associated with these SE sequences, the MAF transcription factor Traffic jam (Tj) emerged as the most prominent binding candidate. With Tj knockdowns in OSS cells, we see a coordinated loss of flam transcripts and piRNAs as well as a decreased expression of many Piwi pathway genes including piwi, which then also coincided with increased transposon RNA levels. We conducted ChIP-seq of Tj’s interaction at Piwi pathway gene promoters and hundreds of other genes important for follicle cell development. Lastly, we utilized transient Tj knockdown in the fly ovary to support our conclusions of how Tj orchestrates the complex Piwi pathway network in Drosophila follicle cells.
2025-04-01 | PXD052946 | Pride
Project description:Transposable elements (TEs) are genomic parasite that threat genome integrity. One major strategy organisms evolved to balance TE activity in the germline is the Piwi-interacting RNAs (piRNAs) pathway. It prevents transposition by repressing TE at transcriptional and/or post-transcriptional level. However, evidence that TE derepression caused by piRNA pathway impairment is actually followed by bursts of transposition is still lacking. Here we present a genome-wide TE-analyses of the replicative TE life cycle (their expression, their translation to their transposition in the germline) after piRNA pathway impairment in the somatic follicle cells. We observed a high transposition-rate in the germline, leading to a 10-fold increase in genomic TE-load after 70 successive generations of piRNA pathway impairment. Moreover, we demonstrate that siRNAs co-regulate TE activity at post transcriptional level in follicle cells. These observations demonstrate that the small RNA-mediated TE repression in follicle cells contribute to genome homeostasis.
2018-08-09 | GSE112971 | GEO
Project description:Flamenco (Flam) is the most prominent piRNA cluster locus expressed in Drosophila ovarian follicle cells, and it is required for female fertility to silence gypsy/mdg4 transposons. To determine how Flam is regulated, we used promoter-bashing reporter assays in OSS cells to uncover novel enhancer sequences within the first exons of Flam. We confirmed the enhancer sequence relevance in vivo with new Drosophila Flam deletion mutants of these regions that compromised Flam piRNA expression and lowered female fertility from activated transposons. Our proteomic analysis of proteins associated with these enhancer sequences discovered the transcription factor Traffic Jam (TJ). Tj knockdowns in OSS cells caused a decrease in Flam transcripts, Flam piRNAs, and multiple Piwi pathway genes. A TJ ChIP-seq analysis from whole flies and OSS cells confirmed TJ binding exactly at the enhancer that was deleted in the new Flam mutant as well as at multiple Piwi pathway gene enhancers. Interestingly, TJ also bound the Long Terminal Repeats of transposons that had decreased expression after Tj knockdowns in OSS cells. Our study reveals the integral role TJ plays in the on-going arms race between selfish transposons and their suppression by the host Piwi pathway and the Flam piRNA cluster locus.
2025-02-02 | GSE286025 | GEO
Project description:Primary piRNAs in Drosophila ovarian somatic cells arise from piRNA cluster transcripts and the 3′ UTRs of a subset of mRNAs, including Traffic jam (Tj) mRNA. However, it is unclear how these RNAs are determined as primary piRNA sources. Here, we identify a cis-acting 100-nt fragment in the Tj 3′ UTR that is sufficient for producing artificial piRNAs from unintegrated DNA. These artificial piRNAs were effective in endogenous gene transcriptional silencing. Yb, a core component of primary piRNA biogenesis center Yb bodies, directly bound the Tj-cis-element. Disruption of this interaction markedly reduced piRNA production. Thus, Yb is the trans-acting partner of the Tj-cis-element. Yb-CLIP revealed that Yb-binding correlated with somatic piRNA production but Tj-cis-element downstream sequences produced few artificial piRNAs. Thus, Yb determines primary piRNA sources by two modes of action; primary binding to cis-elements to specify substrates, and secondary binding to downstream regions to increase diversity in piRNA populations.
2015-06-05 | GSE69625 | GEO
Project description:Primary piRNAs in Drosophila ovarian somatic cells arise from piRNA cluster transcripts and the 3′ UTRs of a subset of mRNAs, including Traffic jam (Tj) mRNA. However, it is unclear how these RNAs are determined as primary piRNA sources. Here, we identify a cis-acting 100-nt fragment in the Tj 3′ UTR that is sufficient for producing artificial piRNAs from unintegrated DNA. These artificial piRNAs were effective in endogenous gene transcriptional silencing. Yb, a core component of primary piRNA biogenesis center Yb bodies, directly bound the Tj-cis-element. Disruption of this interaction markedly reduced piRNA production. Thus, Yb is the trans-acting partner of the Tj-cis-element. Yb-CLIP revealed that Yb-binding correlated with somatic piRNA production but Tj-cis-element downstream sequences produced few artificial piRNAs. Thus, Yb determines primary piRNA sources by two modes of action; primary binding to cis-elements to specify substrates, and secondary binding to downstream regions to increase diversity in piRNA populations. HITS-CLIP of Yb in OSCs (Ovarian Somatic Cells) depleted for tj cis-element, and small RNA sequencing of Piwi-piRNAs in OSCs depleted for tj cis-element.
2015-06-05 | E-GEOD-69625 | biostudies-arrayexpress