In the phytopathogenic fungus Ustilago maydis, fusion of compatible haploid
cells is a prerequisite for infection. This process is genetically control
led by the biallelic a locus, encoding pheromone precursors and receptors.
These are presumed to be coupled to a heterotrimeric G protein and a MAP ki
nase cascade, leading to activation of the HMG domain transcription factor
Prf1. Here, we have demonstrated that putative MAP kinase sites in Prf1 are
required for its activity during mating. In addition, we have identified a
gene, kpp2, which encodes a putative MAP kinase related to Pmk1 of Magnapo
rthe grisea and Fus3p of Saccharomyces cerevisiae. kpp2 deletion mutants ar
e attenuated in several steps of development: cell fusion, induction of phe
romone-responsive genes and pathogenicity. Epistasis analysis shows that kp
p2 does not affect pheromone gene expression through the cAMP signalling ca
scade. Pathogenicity of kpp2 mutants can be partially restored by overexpre
ssing the b genes, indicating a regulation of Prf1 by Kpp2. These data supp
ort the hypothesis that the MAP kinase Kpp2 transmits the pheromone signal.