U2AF2 binds <i>IL7R</i> exon 6 ectopically and represses its inclusion.

ABSTRACT: Interleukin 7 receptor α-chain is crucial for the development and maintenance of T cells and genetically associated with autoimmune disorders including multiple sclerosis (MS). Exon 6 of IL7R encodes for its transmembrane domain and regulated by alternative splicing (AS): Inclusion or skipping of IL7R exon 6 results in membrane-bound or soluble IL7R isoforms, respectively. We previously identified SNP rs6897932 in IL7R exon 6, associated with MS risk, and showed that the risk allele (C) results in increased exon skipping and elevated sIL7R. Elevated levels of sIL7R have been shown to exacerbate the disease in the experimental autoimmune encephalomyelitis mouse model of MS. Here we report two mechanisms by which IL7R exon 6 is controlled. A competition between PT

SUBMITTER: Schott G 

PROVIDER: S-EPMC8051268 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature