The induction of sexual development and virulence in the smut fungus Ustilago maydis depends on Crk1, a novel MAPK protein

  1. Elia Garrido1,
  2. Ute Voß2,
  3. Philip Müller2,
  4. Sonia Castillo-Lluva1,
  5. Regine Kahmann2, and
  6. José Pérez-Martín1,3
  1. 1Departamento de Biotecnología Microbiana, Centro Nacional de Biotecnología CSIC, Campus de Cantoblanco-UAM, 28049 Madrid, Spain; 2Max-Planck-Institut für Terrestrische Mikrobiologie, Abteilung Organismische Interaktionen, Karl-von-Frisch-Strasse, D-35043 Marburg, Germany

Abstract

MAP kinases (mitogen-activated protein kinases) are activated by dual phosphorylation on specific threonine and specific tyrosine residues that are separated by a single residue, and the TXY activation motif is a hallmark of MAP kinases. In the fungus Ustilago maydis, which causes corn smut disease, the Crk1 protein, a kinase previously described to have roles in morphogenesis, carries a TXY motif that aligns with the TXY of MAP kinases. In this work, we demonstrate that Crk1 is activated through a mechanism that requires the phosphorylation of this motif. Our data show that Fuz7, a MAPK kinase involved in mating and pathogenesis in U. maydis, is required to activate Crk1, most likely through phosphorylation of the TXY motif. Consistently, we found that Crk1 is also required for mating and virulence. We investigated the reasons for sterility and avirulence of crk1-deficient cells, and we found that Crk1 is required for transcription of prf1, a central regulator of mating and pathogenicity in U. maydis. Crk1 belongs to a wide conserved protein group, whose members have not been previously defined as MAP kinases, although they carry TXY motifs. On the basis of our data, we propose that all of these proteins constitute a new family of MAP kinases.

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Footnotes

  • Supplemental material is available at http://www.genesdev.org.

  • Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.314904.

  • 3 Corresponding author. E-MAIL: jperez{at}cnb.uam.es; FAX 34-91-585-4506.

    • Accepted October 11, 2004.
    • Received June 28, 2004.
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