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

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. Mechanistica

SUBMITTER: Zhang X 

PROVIDER: S-EPMC8482499 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature