The Role of the Rck1 and Rck2 Kinases in the Osmotic Stress Response of Budding Yeast

Abstract

In response to high extracellular salt levels, Saccharomyces cerevisiae activates the HOG1 mitogen-activated protein kinase (MAPK) cascade, which signals to decrease cell growth and provide a method of survival in osmotic stress. Studies have shown that this occurrence can be attributed to an interaction between Hog1 and TOR (target of rapamycin); however, the method of interaction is unknown. Here, we use microarrays to investigate Rck2, a direct downstream substrate of Hog1, and its close homologue Rck1, as possible intermediates connecting Hog1 and TOR in the osmotic stress response. Our findings demonstrated that Rck1 and Rck2 were not acting in a salt dependent manner; however knocking out these kinases did cause significant changes in gene expression at 2452 genes. Rather, using a gene ontology search program, we found that Rck1 and Rck2 are involved in regulating cell growth, and that they interact with 7 transcription factors: Fhl1, Rap1, Ino2, Hir1, Hir2, Spt2 and YML081W.