Crosstalk between the Ras2p-controlled mitogen-activated protein kinase and cAMP pathways during invasive growth of Saccharomyces cerevisiae

The two highly conserved RAS genes of the budding yeast Saccharomyces cerev isiae are redundant for viability. Here we show that haploid invasive growt h development depends on RAS2 but not RAS1. Ras1p is not sufficiently expre ssed to induce invasive growth. Ras2p activates invasive growth using eithe r of two downstream signaling pathways, the filamentation MAPK (Cdc42p/Ste2 0p /MAPK) cascade or the cAMP-dependent protein kinase (Cyr1p/cAMP/PKA) pat hway. This signal branch point can be uncoupled in cells expressing Ras2p m utant proteins that carry amino acid substitutions in the adenylyl cyclase interaction domain and therefore activate invasive growth solely dependent on the MAPK cascade. Both Ras2p-controlled signaling pathways stimulate exp ression of the filamentation response element-driven reporter gene dependin g on the transcription factors Ste12p and Tec1p, indicating a crosstalk bet ween the MAPK and the cAMP signaling pathways in haploid cells during invas ive growth.