Project description:Analysis of splicing defects in Schizosaccharomyces pombe upon chemical genetic inhibition of splicing kinases dsk1, lkh1, and prp4, as well as alanine-mutation of phosphorylated residues in the splicing factors bpb1, prp2, rsd1, srp1, srp2, usp101, usp103, sum3, prp22, cdc5, and cwf22. This study shows the splicing kinase dsk1 modulates splicing efficiency of introns with non-consensus splice sites, likely through phosphorylation of bpb1. Modulation of splicing efficiency of transcripts through kinase signaling pathways may afford the necessary flexibility to tune the gene expression profile in response to environmental and developmental cues.
