Control of cell cycle progression by the stress-activated Hog1 MAPK

Abstract

Activation of the stress-activated Hog1 kinase is essential for cell survival in response to high osmolarity. The Hog1 SAPK elicits the program for cell adaptation that includes modulation of several aspects of cell biology, such as, gene expression, translation and cell-cycle progression. In response to stress, the Hog1 SAPK mediates a transient cell cycle arrest required for proper cell adaptation. A recent report has described the mechanism underlying the effect of the SAPK at G1. Here, we propose that the mechanisms that involve cell cycle control in response to osmostress are of great complexity and that they could be conserved among eukaryotic cells.