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

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

PROVIDER: PRJNA1251672 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33161200_1.fastq.gz	Fastqsanger.gz
	SRR33161200_2.fastq.gz	Fastqsanger.gz
	SRR33161201_1.fastq.gz	Fastqsanger.gz
	SRR33161201_2.fastq.gz	Fastqsanger.gz
	SRR33161202_1.fastq.gz	Fastqsanger.gz

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

Project description:Sex-lethal is recruited to chromatin to promote neuronal tRNA synthesis in males through RNA Polymerase III regulation

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

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

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Sex-lethal is recruited to chromatin to promote neuronal tRNA synthesis in males through RNA Polymerase III regulation [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 | GSE294835 | GEO

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

2025-04-18 | GSE294837 | GEO

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-04-18 | GSE294838 | 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.

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

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

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Cdk1 gates cell cycle-dependent tRNA synthesis by regulating RNA polymerase III activity.

Project description:tRNA genes are transcribed by RNA polymerase III (RNAPIII). During recent years it has become clear that RNAPIII activity is strictly regulated by the cell in response to environmental cues and the homeostatic status of the cell. However, the molecular mechanisms that control RNAPIII activity to regulate the amplitude of tDNA transcription in normally cycling cells are not well understood. Here, we show that tRNA levels fluctuate during the cell cycle and reveal an underlying molecular mechanism. The cyclin Clb5 recruits the cyclin dependent kinase Cdk1 to tRNA genes to boost tDNA transcription during late S phase. At tDNA genes, Cdk1 promotes the recruitment of TFIIIC, stimulates the interaction between TFIIIB and TFIIIC, and increases the dynamics of RNA polymerase III in vivo. Furthermore, we identified Bdp1 as a putative Cdk1 substrate in this process. Preventing Bdp1 phosphorylation prevented cell cycle-dependent recruitment of TFIIIC and abolished the cell cycle-dependent increase in tDNA transcription. Our findings demonstrate that under optimal growth conditions Cdk1 gates tRNA synthesis in S phase by regulating the RNAPIII machinery, revealing a direct link between the cell cycle and RNAPIII activity.

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RNAseq of old and young males with equal physical activity

Project description:18 older (65-71 years) and 20 young (19-25 years) males were recruited based on similar, self-reported physical activity, which was verified using accelerometry measurements. Gene expression profiles of vastus lateralis biopsies obtained by RNA sequencing. A clear ageing signature was observed despite similar physcical activity.

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