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Drosophila melanogaster

ABSTRACT: Flipping the switch on Sex-lethal expression: Sister of Sex-lethal antagonizes Sxl-dependent alternative splicing to maintain a male-specific gene expression pattern in Drosophila (iCLIP)

PROVIDER: PRJNA384220 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5480970.fastq.gz	Fastqsanger.gz
	SRR5480967.fastq.gz	Fastqsanger.gz
	SRR5480968.fastq.gz	Fastqsanger.gz
	SRR5480969.fastq.gz	Fastqsanger.gz

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Similar Datasets

Flipping the switch on Sex-lethal expression: Sister of Sex-lethal antagonizes Sxl-dependent alternative splicing to maintain a male-specific gene expression pattern in Drosophila

Project description:Flipping the switch on Sex-lethal expression: Sister of Sex-lethal antagonizes Sxl-dependent alternative splicing to maintain a male-specific gene expression pattern in Drosophila

| PRJNA384219 | ENA

Flipping the switch on Sex-lethal expression: Sister of Sex-lethal antagonizes Sxl-dependent alternative splicing to maintain a male-specific gene expression pattern in Drosophila (iCLIP)

Project description:In Drosophila female development is governed by a single RNA-binding protein, Sex lethal (Sxl), that controls the expression of key factors involved in dosage compensation, germline homeostasis and the establishment of female morphology and behaviour. Functional Sxl protein is only synthesized in female flies. Its expression is established in the pre-cellular, female embryo by an X-chromosome counting mechanism and maintained by a positive feedback loop with Sxl controlling alternative splicing of its own transcript. In male flies this feedback loop is not activated, keeping Sxl expression in the ‘off’ state. But what protects males against accidental triggering of the self-sustaining feedback loop and Sxl protein production snowballing out of control? Here we identify Sister of sex lethal (Ssx) as a protein that antagonizes Sxl in autoregulatory splicing by competition for the same RNA elements. Male flies mutant for ssx exhibit a low level of productive Sxl mRNA splicing and in cultured Drosophila cells, Sxl-induced changes in alternative splicing can be reverted by the expression of Ssx. In sum, this demonstrates that Ssx helps to establish a stable, male-specific gene expression pattern by protecting male flies against triggering Sxl expression.

2019-01-15 | GSE98188 | GEO

Flipping the switch on Sex-lethal expression: Sister of Sex-lethal antagonizes Sxl-dependent alternative splicing to maintain a male-specific gene expression pattern in Drosophila (RIP-Seq)

2019-01-15 | GSE98187 | GEO

Drosophila melanogaster

| PRJNA384221 | ENA

Effects of Sxl on gene expression in the male head of Drosophila

Project description:Sex-lethal (Sxl), a feminizing switch gene in Drosophila, also generates male-specific proteins and non-sex-specific mRNAs, despite the fact that deleting the gene from males causes no obvious phenotypic abnormalities. We specifically investigate how Sxl may affect gene expression in the male head, where SXL isoforms have been detected. The information may help us understand how Sxl acquired its functional roles in sex determination during evolution in Drosophila Keywords: Comparative expression, genetic modification

2008-12-30 | GSE9571 | GEO

Sex Lethal is recruited to chromatin by RNA polymerase III [DamID-seq]

Project description:We discovered that the splicing factor Sex lethal (Sxl) also associates strongly with chromatin and that this association is not linked to its RNA-binidng capacity, nor its N- or C-terminal domains. We also found that Sxl is recruited to chromatin by the RNA polymerase III subunt Polr3E.

2025-04-18 | GSE239790 | GEO

Sex-lethal regulates back-splicing and generation of the sex-differentially expressed circular RNAs

Project description:Conversely to canonical splicing, back-splicing covalently ligates the upstream 3' splice site (SS) with downstream 5'SS and generates exonic circular RNAs (circRNAs) that are widely-identified in eukaryotes and have regulatory functions in gene expression. However, sex-specific back-splicing in Drosophila has not been investigated and its regulation remains unclear. Here, we performed multiple RNA-seq of various sex-specific Drosophila samples including head, body and gonads from both genders, and identified more than ten thousand of circular RNAs, in which hundreds are sex-differentially expressed and back-spliced. Intriguingly, we found that expression of SXL, an RNA-binding protein encoded by Sex-lethal (Sxl), the master Drosophila sex-determination gene which only functionally spliced in females, promotes back-splicing of many female-differentially expressed circRNAs in the male S2 cells, while expression of a SXL mutant did not. Using a monoclonal antibody, we further obtained the transcriptome-wide RNA-binding sites of SXL through a PAR-CLIP approach and revealed that SXL-binding on flanking exons and introns of pre-mRNAs facilitates back-splicing of those circRNAs, whereas SXL-binding on the circRNA exons inhibits the back-splicing. This study provides strong evidence that SXL has a regulatory role in back-splicing to generate sex-specifc circRNAs, as well as in the initiation of Drosophila sex-determination cascade through canoncial forward-splicing.

2023-04-23 | GSE221102 | GEO

Sex-lethal is recruited to chromatin to promote neuronal tRNA synthesis in males through RNA Polymerase III regulation [small RNA-seq]

Project description:The RNA-binding protein sex-lethal (Sxl) is classically defined as a master regulator of sex determination and RNA splicing in Drosophila melanogaster. However, this role is not conserved in all species and functions beyond this canonical pathway remain largely unexplored. Here, we uncover a splicing-independent function for Sxl at the chromatin level in the Drosophila brain. Using Targeted DamID (TaDa) profiling in larval neurons, we identify widespread recruitment of Sxl to promoter regions, independent of sex and RNA binding activity. Notably, Sxl chromatin occupancy exhibits near-complete overlap with Polr3E (RPC37), an RNA Polymerase III subunit, with Sxl binding abolished upon Polr3E knockdown. Depletion of Sxl in mature male neurons equally induces widespread transcriptional changes, particularly in metabolic genes, and improves negative geotaxis during ageing, phenotypes that closely mirror Polr3E knockdown. Conversely, overexpression of SxlRAC isoform enhances tRNA synthesis and upregulates metabolic gene expression. Together, these findings reveal a previously unrecognised role for Sxl in regulating Pol III activity via Polr3E, promoting tRNA synthesis and supporting neuronal metabolism. Given the emerging tie between Pol III regulation and neuronal ageing, our study highlights Sxl as a novel modulator of neuronal homeostasis.

2025-04-18 | GSE294837 | GEO

Sex-lethal is recruited to chromatin to promote neuronal tRNA synthesis in males through RNA Polymerase III regulation [RNA-seq]

2025-04-18 | GSE294835 | GEO

Sex-specific development in haplodiploid honeybee is controlled by the female-embryo-specific activation of thousands of intronic lncRNAs

Project description:Sex determination in the honeybee (Apis mellifera) is governed by the queen-controlled unfertilization or fertilization of embryo, though the mechanisms of determination are poorly understood. Here, we obtained the transcriptomes from individual worker and drone embryo during the embryonic development (day 1 to day 3). We show that transcriptional difference between worker and drone embryo is very small during the first day of hatching, during which sex-determinant gene csd expresses similarly. Differential transcription between worker and drone embryo bursts at day 2, among which csd is induced in worker embryo at day 2 and sex-lethal gene sxl is repressed in male embryo. An unexpected global regulation of alternative splicing accompanies the honeybee embryonic development, and male and worker embryo show distinct regulatory patterns and mechanisms. This study suggests the honeybee sex determination is more globally controlled at both the transcriptional and alternative splicing levels.

2021-07-27 | GSE101741 | GEO

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