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  • Splicing factor Srsf5 deletion disrupts alternative splicing and causes noncompaction of ventricular myocardium.

Splicing factor Srsf5 deletion disrupts alternative splicing and causes noncompaction of ventricular myocardium.

iScience (2021-10-09)
Xiaoli Zhang, Ze Wang, Qing Xu, Yuhan Chen, Wen Liu, Tong Zhong, Hongchang Li, Chengshi Quan, Lingqiang Zhang, Chun-Ping Cui
ABSTRACT

The serine/arginine-rich (SR) family of splicing factors plays important roles in mRNA splicing activation, repression, export, stabilization, and translation. SR-splicing factor 5 (SRSF5) is a glucose-inducible protein that promotes tumor cell growth. However, the functional role of SRSF5 in tissue development and disease remains unknown. Here, Srsf5 knockout (Srsf5 -/- ) mice were generated using CRISPR-Cas9. Mutant mice were perinatally lethal and exhibited cardiac dysfunction with noncompaction of the ventricular myocardium. The left ventricular internal diameter and volume were increased in Srsf5 -/- mice during systole. Null mice had abnormal electrocardiogram patterns, indicative of a light atrioventricular block. Mechanistically, Srsf5 promoted the alternative splicing of Myom1 (myomesin-1), a protein that crosslinks myosin filaments to the sarcomeric M-line. The switch between embryonic and adult isoforms of Myom1 could not be completed in Srsf5-deficient heart. These findings indicate that Srsf5-regulated alternative splicing plays a critical role during heart development.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Anti-SRSF5 antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Sigma-Aldrich
EZ-Magna NuCLEAR RIP (Cross-Linked) Nuclear RNA-Binding Protein Immunoprecipitation Kit, EZ-Magna Nuclear RIP (Cross-Linked) RNA-Binding Protein Immunoprecipitation Kit is designed for the analysis of chromatin associated RNA such lncRNAs, enhancer RNAs and miRNAs.