p38 SAPK and SKIIP induced changes in alternative splicing patterns upon osmostress

Alternative splicing is a crucial mechanism for gene regulation that is modulated in response to a wide range of extracellular stimuli. Stress-activated protein kinases (SAPKs) play a key role in controlling several steps of mRNA biogenesis. Here, we show that osmostress has a major impact on the regulation of alternative splicing (AS), which is partly mediated through the action of the p38 SAPK. Remarkably, a splicing network analysis revealed a functional connection between p38 and the spliceosome component SKIIP. Depletion of SKIIP abolished a significant part of the p38-mediated alternative splicing. Overall design: Alternative Splicing analysis of non-treated, stressed, and stressed cells pre-treated with the p38 SAPK inhibitor under control or SKIIP knock down conditions. Sequencing Core Facility: CRG