Distinct signalling pathways coordinately contribute to virulence of Fusarium oxysporum on mammalian hosts

Rafael C. Prados-Rosales, Carolina Serena, Jesús Delgado-Jarana, Josep Guarro, Antonio Di Pietro

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

The filamentous fungus Fusarium oxysporum causes vascular wilt on a wide range of plant species and is an emerging pathogen of humans. A mitogen-activated protein kinase, Fmk1, and a G protein β subunit, Fgb1, control pathogenicity of F. oxysporum on plants through distinct signalling pathways. In the present report, we studied the genetic interaction between fmk1 and fgb1 and their role in virulence on a mammalian host. The Δfmk1 or Δfgb1 single mutants exhibited similar virulence patterns as the wild type strain in an immunodepressed mouse model. By contrast, double mutants lacking both genes had dramatically reduced virulence. All mutants showed similar in vitro growth or tolerance to temperature and osmotic stress as the wild type strain. However, the Δfgb1 and Δfmk1 strains were reduced in specific extracellular protease activity or adhesion to fibronectin, respectively, two factors previously associated with fungal virulence. Thus, Fmk1 and Fgb1 are components of distinct signalling pathways which collectively control virulence of F. oxysporum on mammalian hosts.

Original languageEnglish (US)
Pages (from-to)2825-2831
Number of pages7
JournalMicrobes and Infection
Volume8
Issue number14-15
DOIs
StatePublished - Nov 1 2006

Keywords

  • Adhesion
  • Fibronectin
  • G β subunit
  • Hydrophobicity
  • MAP kinase
  • Murine model
  • Protease
  • cAMP

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Infectious Diseases

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    Prados-Rosales, R. C., Serena, C., Delgado-Jarana, J., Guarro, J., & Di Pietro, A. (2006). Distinct signalling pathways coordinately contribute to virulence of Fusarium oxysporum on mammalian hosts. Microbes and Infection, 8(14-15), 2825-2831. https://doi.org/10.1016/j.micinf.2006.08.015