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Vol. 10, Issue 5, 1325-1335, May 1999

Crosstalk between the Ras2p-controlled Mitogen-activated Protein Kinase and cAMP Pathways during Invasive Growth of Saccharomyces cerevisiae

Hans-Ulrich Mösch,* Eric Kübler,* Sven Krappmann,* Gerald R. Fink,dagger and Gerhard H. Braus*Dagger

 *Institute for Microbiology and Genetics, Georg-August-University, D-37077 Göttingen, Germany; and  dagger Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142

The two highly conserved RAS genes of the budding yeast Saccharomyces cerevisiae are redundant for viability. Here we show that haploid invasive growth development depends on RAS2 but not RAS1. Ras1p is not sufficiently expressed to induce invasive growth. Ras2p activates invasive growth using either of two downstream signaling pathways, the filamentation MAPK (Cdc42p/Ste20p/MAPK) cascade or the cAMP-dependent protein kinase (Cyr1p/cAMP/PKA) pathway. This signal branch point can be uncoupled in cells expressing Ras2p mutant 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 expression of the filamentation response element-driven reporter gene depending on the transcription factors Ste12p and Tec1p, indicating a crosstalk between the MAPK and the cAMP signaling pathways in haploid cells during invasive growth.


Dagger    Corresponding author: E-mail address: gbraus{at}gwdg.de.


Molecular Biology of the Cell
Vol. 10, 1325-1335, May 1999
Copyright © 1999 by The American Society for Cell Biology



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