Project description:ABSTRACT: Condensin is a central regulator of mitotic genome structure, with mutants showing poorly condensed chromosomes and profound segregation defects. Here we identify the fission yeast NCT complex, comprising the Nrc1 BET-family tandem bromodomain protein (SPAC631.02), Casein Kinase II (CKII) and several TAFs, as a novel regulator of condensin function (where NCT mutants restore the formation of segregation-competent chromosomes in cells containing defective condensin). Synchronous ChIP-seq shows that NCT and condensin bind similar genomic regions, but only briefly co-localize during the periods of chromosome condensation and decondensation. These results are consistent with a model where NCT targets CKII to chromatin in a cell cycle-directed manner to modulate the activity of condensin during chromosome condensation and decondensation. DATA: Study includes ChIP-seq of fission yeast H3-K4Me3, H3-K36Me3, TBP, Taf7, Nrc1, Cka1 from aynchronous cells; Nrc1 and Cut3 (representing condensin) from four synchronized cell-cycle stages estimated as G2/M, Metaphase, Anaphase and G1/S.
Project description:ABSTRACT: Condensin is a central regulator of mitotic genome structure, with mutants showing poorly condensed chromosomes and profound segregation defects. Here we identify the fission yeast NCT complex, comprising the Nrc1 BET-family tandem bromodomain protein (SPAC631.02), Casein Kinase II (CKII) and several TAFs, as a novel regulator of condensin function (where NCT mutants restore the formation of segregation-competent chromosomes in cells containing defective condensin). Synchronous ChIP-seq shows that NCT and condensin bind similar genomic regions, but only briefly co-localize during the periods of chromosome condensation and decondensation. These results are consistent with a model where NCT targets CKII to chromatin in a cell cycle-directed manner to modulate the activity of condensin during chromosome condensation and decondensation.
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.
