Abstract
Isoamyl alcohol (IAA) induces a phenotype that resembles pseudohyphae in the budding yeast Saccharomyces cerevisiae. We show here that IAA causes the rapid formation of linear chains of anucleate buds, each of which is accompanied by the formation of a septin ring at its neck. This process requires the activity of Swe1 and Slt2 (Mpk1). Cdc28 is phosphorylated on tyrosine 19 in a Swe1-dependent manner, while Slt2 becomes activated by dual tyrosine/threonine phosphorylation. Tyrosine 19 phosphorylation of Cdc28 is not dependent on Slt2. However, the defective response in the slt2Delta mutant is rescued by an mih1Delta mutation. The IAA response still occurs in a cell containing a dominant non-phosphorylatable form of Cdc28, but no longer occurs in an mih1Delta slt2Delta mutant containing this form of Cdc28. These observations show that IAA induces the Swe1-dependent morphogenesis checkpoint and so the resulting pseudohyphal phenotype arises in an entirely different way from the formation of pseudohyphae induced by nitrogen-limited growth.
Highlights
The yeast Saccharomyces cerevisiae can grow either in a unicellular budding form or in branching chains of elongated cells known as pseudohyphae (Gimeno et al, 1992)
The defective response in the slt2∆ mutant is rescued by an mih1∆ mutation
The isoamyl alcohol (IAA) response still occurs in a cell containing a dominant nonphosphorylatable form of Cdc28, but no longer occurs in an mih1∆ slt2∆ mutant containing this form of Cdc28
Summary
The yeast Saccharomyces cerevisiae can grow either in a unicellular budding form or in branching chains of elongated cells known as pseudohyphae (Gimeno et al, 1992). Pseudohyphae form in diploids in response to nitrogen-limited growth, and in other stress and starvation conditions. Two signal transduction pathways are required involving the mating pheromone MAP kinase module and cAMP/PKA, respectively. These pathways converge on elements in the complex promoters of genes such as FLO11. Filamentous growth requires an extended G2 and a delay in the switch from polarised to isotropic growth of the bud (Kron et al, 1994). This involves inhibition of the activity of the Clb2-Cdc kinase, but the way in which this comes about is currently unclear. It is known that it does not depend upon inhibitory tyrosine phosphorylation by Swe, because pseudohypha formation occurs normally during nitrogenlimited growth in a swe1∆ mutant (Ahn et al, 1999)
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