LOSS OF GIT1 GENE IN FISSION YEAST PROVIDES RESISTANCE TO ENDOPLASMIC RETICULUM STRESS

Abstract

Schizosaccharomyces pombe detects glucose G-protein coupled receptor and transmits signal transduction via a cAMP-dependent protein kinase A (PICA) pathway. Also, Git1 C2 domain protein is required for maintaining basal cAMP levels and for producing glucose-triggered cAMP response. Actually, Git1 is a member of the UNC-13/Munc13 protein family that are conserved in eukaryotes and functionally included in synaptic vesicle exocytosis. We aimed to investigate the impact of Git1 on the vesicular trafficking dependent on endoplasmic reticulum and on the oxidative stress response. In this study, we cloned the full-length (git1T) of S. pombe girl gene into pSGP572 plasmid, as a S. pombe expression vector carrying thiamine repressed promoter, nmt1 and C-terminal GFP. Then, we compared the viability of S. pombe strains (wild type, git Delta, pSGP572/git Delta, pG1T/git Delta) against to H2O2-induced oxidative stress and tunicamycin-induced ER stress to that of their control groups. We found that deletion of git1 gene brought S. pombe resistance to ER stress, but not oxidative stress in S. pombe cells.