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.
Project description:Puf3 is a RNA-binding protein, a member of the conserved Puf-protein family. Combining different functional genomics data, we have analyzed the role of Puf3 in post-transcriptional gene regulation in S. pombe. We present data on Puf3 interacting proteins and regulatory mRNA targets.
Project description:Nitric oxide being a versatile molecule inside biological systems, from being both a cell signaling molecule to a potent stress agent, has significant effect in the transcriptional response in fission yeast. We have used fission yeast microarrays to identify cellular targets of Nitric Oxide (NO) and to further understand the cellular mechanism of NO action. We report the change in the global gene expression profile response to NO in S. pombe cells S. pombe cells were treated with pure NO donor compond detaNONOate for 15 minutes at 30 degrees celcius for both the wild type and pap1 deleted strain, the cells were processed through RNA extraction and hybridization on Affymetrix microarrays. We included pap1 deleted strain of S. pombe alongside wild type strain as we earlier reported that pap1 is important to combat nitrosative stress, so pap1 might control the expression of several genes under nitrosative stress. Wild type control and treated samples as well as Mutant control and treated sets are included in 2 biological replicates for each.