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Negative autoregulation of BMP dependent transcription by SIN3B splicing reveals a role for RBM39

ABSTRACT: Negative autoregulation of BMP dependent transcription by SIN3B splicing reveals a role for RBM39

PROVIDER: PRJNA808989 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18088202_1.fastq.gz	Fastqsanger.gz
	SRR18088202_2.fastq.gz	Fastqsanger.gz
	SRR18088203_1.fastq.gz	Fastqsanger.gz
	SRR18088203_2.fastq.gz	Fastqsanger.gz
	SRR18088204_1.fastq.gz	Fastqsanger.gz

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Negative autoregulation of BMP dependent transcription by SIN3B splicing reveals a role for RBM39

Project description:We conducted RNASeq using mRNA extracted from C2C12 mouse myoblast cells transfected with non-targeting control (NTC) or RBM39 siRNA, to elucidate the effect of RBM39 on regulation of BMP4 pathway

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Negative autoregulation of BMP dependent transcription by SIN3B splicing reveals a role for RBM39.

Project description:BMP signalling is negatively autoregulated by several genes including SMAD6, Noggin and Gremlin, and autoregulators are possible targets for enhancing BMP signalling in disorders such as fibrosis and pulmonary hypertension. To identify novel negative regulators of BMP signalling, we used siRNA screening in mouse C2C12 cells with a BMP-responsive luciferase reporter. Knockdown of several splicing factors increased BMP4-dependent transcription and target gene expression. Knockdown of RBM39 produced the greatest enhancement in BMP activity. Transcriptome-wide RNA sequencing identified a change in Sin3b exon usage after RBM39 knockdown. SIN3B targets histone deacetylases to chromatin to repress transcription. In mouse, Sin3b produces long and short isoforms, with the short isoform lacking the ability to recruit HDACs. BMP4 induced a shift in SIN3B expression to the long isoform, and this change in isoform ratio was prevented by RBM39 knockdown. Knockdown of long isoform SIN3B enhanced BMP4-dependent transcription, whereas knockdown of the short isoform did not. We propose that BMP4-dependent transcription is negatively autoregulated in part by SIN3B alternative splicing, and that RBM39 plays a role in this process.

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Project description:Pharmacologic depletion of RNA-binding motif 39 (RBM39) using aryl sulfonamides represents a promising anti-cancer therapy but requires high levels of the adaptor protein DCAF15. Consequently, novel approaches to deplete RBM39 in an DCAF15-independent manner are required. Here, we uncover that RBM39 autoregulates via the inclusion of a poison exon into its own pre-mRNA and identify the cis-acting elements that govern this regulation. We also determine the NMR solution structures of RBM39's tandem RNA recognition motifs (RRM1 and RRM2) bound to their respective RNA targets, revealing how RRM1 recognises RNA stem loops whereas RRM2 binds specifically to single-stranded N(G/U)NUUUG. Our results support a model where RRM2 selects the 3'-splice site of a poison exon and the RRM3 and RS domain stabilise the U2 snRNP at the branchpoint. Our work provides molecular insights into RBM39-dependent 3'-splice site selection and constitutes a solid basis to design alternative anti-cancer therapies.

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