Elements of a single MAP kinase cascade in Saccharomyces cerevisiae mediate two developmental programs in the same cell type: mating and invasive growth.

Abstract

Diploid Saccharomyces cerevisiae strains starved for nitrogen undergo a developmental transition from a colonial form of growth to a filamentous pseudohyphal form. This dimorphism requires a polar budding pattern and elements of the MAP kinase signal transduction pathway essential for mating pheromone response in haploids. We report here that haploid strains exhibit an invasive growth behavior with many similarities to pseudohyphal development, including filament formation and agar penetration. Haploid filament formation depends on a switch from an axial to a bipolar mode of bud site selection. Filament formation is distinct from agar penetration in both haploids and diploids. We find that the same components of the MAP kinase cascade necessary for diploid pseudohyphal development (STE20, STEI1, STE7, and STE12) are also required for both filament formation and agar penetration in haploids. Thus, haploid yeast cells can enter either of two developmental pathways: mating or invasive growth, both of which depend on elements of a single MAP kinase cascade. Our results provide a novel developmental model to study the dynamics of signal transduction, with implications for higher eukaryotes.

In Saccharomyces cerevisiae an unbalanced level of tyrosine phosphorylation down-regulates the Ras/PKA pathway

“…The invasive growth assay was performed as previously described (Roberts & Fink, 1994). Briefly, cells were spotted on YPD plates, incubated at 30 • C for 3 days and for an additional 2 days at 24 • C. Plates were then photographed, washed with a gentle stream of deionized water and photographed again.…”

“…Different environmental stimuli induce dimorphic switch in haploids (invasive growth) and diploids (pseudohyphal growth) cells. The triggering signal appears to be glucose starvation in haploids (Cullen & Sprague, 2000;Roberts & Fink, 1994) and nitrogen starvation in diploids (Gimeno et al, 1992). In both cases, a major alteration in cell morphology is observed so that cells become elongated and do not separate after cytokinesis, generating cell chains that invade the growth substrate.…”

The control of morphogenesis in Saccharomyces cerevisiae by Elm1 kinase is responsive to RAS/cAMP pathway activity and tryptophan availability

“…shr3 cells, in which amino acid transport is severely compromised because amino acid permeases are not transported to the cell membrane , exhibit enhanced filamentous growth on SLAD. The nutritional signals triggering haploid invasive growth are even less well understood, as this phenomenon has been observed in mature colonies on rich media (Roberts and Fink, 1994). The nutritional status of the cells initiating invasive growth at the base of these colonies is completely unknown, and they may well be severely limited for certain nutrients.…”

Genomewide mechanisms of chronological longevity by dietary restriction in budding yeast

“…Among the top hits of our DR regulator analysis was Ste12, a transcription factor acting on genes involved in mating or pseudohyphal growth (Dolan, Kirkman & Fields, 1989; Roberts & Fink, 1994). STE12 is an important regulatory hub during stationary phase (Wanichthanarak, Wongtosrad & Petranovic, 2015); however, its role in stationary‐phase survival in response to nutrients has not been confirmed, as opposed to other hits such as Msn2 and Msn4 (Fabrizio et al., 2004).…”

“…Ste12 acts downstream of two cell differentiation programs regulated by MAPK pathways, namely mating and invasive growth (Dolan et al., 1989; Roberts & Fink, 1994). Not only the ste12 Δ strain showed diminished longevity under different experimental settings, but also STE12 overexpression was sufficient to extend lifespan under a nonrestricted diet.…”