Pseudohyphal growth in both haploid and diploid strains of Saccharomyces ce
revisiae reflects concerted changes in different cellular processes: buddin
g pattern, cell elongation and cell adhesion. These changes are triggered b
y environmental signals and are controlled by several pathways which act in
parallel. Nitrogen deprivation, and possibly other stresses, activate a MA
P kinase cascade which has the transcription factor Ste12 as its final targ
et. A cAMP-dependent pathway, in which the protein kinase Tpk2 plays a spec
ific role, is also required for the morphogenetic switch. Both pathways con
tribute to modulate the expression of the MUC1/FLO11 gene which encodes a c
ell-surface flocculin required for pseudohyphal and invasive growth. The MA
P kinase cascade could also control the activity of the cyclin/ Cdc28 compl
exes which affect both the budding pattern of yeast and cell elongation. A
further protein which stimulates filamentous growth in S, cerevisiae is Phd
1, although its mode of action is unknown, it may be regulated by a cAMP-de
pendent protein kinase, as occurs with the homologous protein Efg1 from Can
dida albicans, which is required for the formation of true hyphae. Morphoge
nesis in different yeast genera share common elements, but there are also i
mportant differences. Although a complete picture cannot yet be drawn, part
ial models may be proposed for the interaction of the regulatory pathways,
both in the case of S. cerevisiae and in that of C. albicans. (C) 2001 Fede
ration of European Microbiological Societies. Published by Elsevier Science
B.V. All rights reserved.