Abstract #269

Antagonistic growth regulation by HOG pathway and Ca ²⁺ signaling pathways in budding yeast.
Atsunori Shitamukai (1), Dai Hirata (2), Shinya Sonobe (2), Tokichi Miyakawa (3)
(1) Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University; (2) ; (3) Molecular Biotechnology, Hiroshima University, Kagamiyama, 1-4-1, Higashi-Hiroshima, 739-8527, Japan

The Ca²⁺ signaling pathways of budding yeast, involving calcineurin and the Mpk1 MAP kinase cascade, are implicated in the G2 cell cycle regulation. The simultaneous deletion of these pathways causes lethality, indicating that these branches perform redundant functions in essential events for cell growth. To further clarify the events that are regulated by these pathways, we screened for high-copy suppressor cDNA that can rescue the lethality of the cnb1mpk1 double deletion. One of the isolates contained a PTC4 cDNA encoding a protein phosphatase belonging to the PP2C family. Overexpression of PTC4 led to decreased phosphorylation of Hog1, and HOG1 deletion remarkably suppressed the synthetic lethality of the cnb1mpk1 double deletion, indicating antagonistic roles of the HOG pathway and the signaling pathway in cell growth. The hog1 strain showed hypersensitivity to Ca²⁺, inducing a delay in G2 phase and polarized bud growth. The inhibitory effects of Ca²⁺ were partially rescued by the deletion of calcineurin, but not Mpk1. In a synchronous cell culture, we found that both bud formation and the onset of mitosis were regulated negatively by Ca²⁺ signaling pathways and positively by HOG pathway. It was also found that calcineurin negatively regulates the Ca²⁺-activated Hog1 by up-regulating the transcription of PTP2, negative regulator of the HOG pathway, in a manner mediated by Crz1, calcineurin-regulated transcription factor.

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