A novel function of Saccharomyces cerevisiae PKC1 in the regulation of polarized bud growth.
Masaki Mizunuma, Dai Hirata, Tokichi Miyakawa
Molecular Biotechnology, Hiroshima University, Kagamiyama 1-3-1, Higashi-Hiroshima, 739-8530, Japan (mmizu@hiroshima-u.ac.jp)

Protein kinase C (PKC) signaling is highly conserved among eukaryotes and has been implicated in the regulation of cellular processes such as cell proliferation and polarized growth. In Saccharomyces cerevisiae, the Pkc1/MAP kinase pathway is implicated in promoting bud emergence at the G₁/S transition and in cell wall construction. The calcium-activated pathways of S. cerevisiae induce a delay in the onset of mitosis through the activation of Swe1p, the negative regulatory kinase that inhibits the Cdc28p/Clbp complex. We describe here a genetic approach to identify the components of the Ca²⁺-signaling pathways by screening for mutations that disrupt the Ca²⁺-induced G₂ arrest (designated as scz1~14). Here, we found that Pkc1p is involved in the maintenance of actin polarization and polarized bud growth by regulating the expression of the G₁ cyclins in a manner independent of the Mpk1p MAP kinase pathway. The activation of Ca²⁺ signaling delayed the switch from the polar to the isotropic bud growth by activating Swe1p kinase in a Pkc1p-dependent manner. We propose a novel Pkc1p-mediated mechanism for polarizing bud growth through the activation of Cdc28p-Cln2p and the inhibition of Cdc28p-Clb2p.

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