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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [shRBM39 mRNA-seq]

ABSTRACT: To investigate the role RBM39 plays in alternative splicing, we generated SW480 cell lines in which RBM39 was knocked down by shRNA.We then performed RNA-seq data for alternative splicing gene analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE246915 | GEO | 2024/08/02

REPOSITORIES: GEO

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			Action	DRS
		Other
	GSE246915_ASEvent_summary.txt.gz	Txt
	GSE246915_All_reads_counts.txt.gz	Txt
	GSE246915_All_samples_rpkm.txt.gz	Txt
	GSE246915_TargetAndJunction_event_records.txt.gz	Txt

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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [shMORC2 mRNA-seq]

Project description:To investigate the role MORC2 plays in alternative splicing, we generated SW480 cell lines in which MORC2 was knocked down by shRNA.We then performed RNA-seq data for alternative splicing gene analysis.

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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [RBM39 RIP-seq]

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Global Regulation of Alternative RNA Splicing by the SR-Rich Protein RBM39

Project description:RBM39 is extensively involved in alternative splicing of RNA and helps regulate transcript levels. RBM39 may modulate alternative splicing similarly to U2AF65 by either directly binding to RNA or recruiting other splicing factors, such as U2AF65.

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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [RBM39 RIP-seq]

Project description:MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [RBM39 RIP-seq]

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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer

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RBM39 Modulates UPR Signaling Through Alternative Splicing of IRE1α/ERN1 [siERN1_Rescue_RNA-Seq]

Project description:The unfolded protein response (UPR) preserves endoplasmic reticulum proteostasis through coordinated signaling pathways, including the IRE1α-XBP1 axis, which promotes adaptive transcriptional programs via non-canonical XBP1 mRNA splicing. However, upstream mechanisms regulating this pathway remain incompletely defined. Here, we apply CRASP-Seq, a scalable RNA-coupled CRISPR screening platform, to systematically identify regulators of XBP1 splicing. We uncover the U2 snRNP auxiliary factor RBM39 as a critical positive regulator of this process. Perturbation of RBM39 or U2 snRNP components induces alternative splicing of ERN1, leading to exon-18 skipping and the production of an unstable transcript subject to nonsense-mediated decay, as well as a truncated IRE1α isoform that acts in a dominant-negative manner to suppress XBP1 splicing. Mechanistically, we show that heat shock reduces RBM39 functional activity and promotes ERN1 exon-18 skipping, thereby attenuating IRE1α–XBP1 signaling. Functionally, hyperactivation of this pathway is detrimental under proteotoxic stress, suggesting that exon-18 skipping serves as a stress-adaptive mechanism to limit UPR output. Together, our findings reveal a previously unrecognized regulatory axis linking the canonical splicing machinery to UPR signaling and establish alternative splicing of ERN1 as a key modulator of cellular stress responses.

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