Neuronal SAM68 differentially regulates alternative last exon splicing and ensures proper synapse development and function.

ABSTRACT: Alternative splicing in the 3'UTR of mammalian genes plays a crucial role in diverse biological processes, including cell differentiation and development. SAM68 is a key splicing regulator that controls the diversity of 3'UTR isoforms through alternative last exon (ALE) selection. However, the tissue/cell type-specific mechanisms underlying the splicing control at the 3' end and its functional significance remain unclear. Here, we show that SAM68 regulates ALE splicing in a dose-dependent manner and the neuronal splicing is differentially regulated depending on the characteristics of the target transcript. Specifically, we found that SAM68 regulates interleukin-1 receptor-associated protein splicing through the interaction with U1 small nuclear ribonucleoprotein. In contrast, the ALE splic

SUBMITTER: Darwish M 

PROVIDER: S-EPMC10562862 | biostudies-literature | 2023 Oct

REPOSITORIES: biostudies-literature