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Vol. 10, Issue 5, 1325-1335, May 1999
and
*Institute for Microbiology and Genetics, Georg-August-University,
D-37077 Göttingen, Germany; and 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.
Whitehead Institute
for Biomedical Research, Cambridge, Massachusetts 02142
Corresponding author: E-mail address:
gbraus{at}gwdg.de.
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