Identification of a motor protein required for filamentous growth in Ustilago maydis

C Lehmler1, G Steinberg, K M Snetselaar

  • 1Institut für Genetik und Mikrobiologie der Universität München, Germany.

The EMBO Journal
|June 1, 1997
PubMed

Insights

The kinesin motor protein Kin2 is essential for the pathogenic filamentous growth of Ustilago maydis. Deleting kin2 disrupts hyphal extension and pathogenicity by affecting vesicle transport at the hyphal tip.

Area of Science:

  • Mycology
  • Molecular Biology
  • Plant Pathology

Background:

  • Ustilago maydis exhibits dimorphism, switching between yeast-like haploid and pathogenic filamentous dikaryon stages.
  • Pathogenicity and dimorphism are regulated by mating-type loci, with only the filamentous form infecting corn.

Purpose of the Study:

  • To investigate the role of kinesin motor proteins in Ustilago maydis development and pathogenicity.
  • To identify specific kinesin genes involved in fungal growth and infection.

Main Methods:

  • Gene identification and deletion mutant construction (kin1, kin2).
  • Phenotypic analysis of mutants, including hyphal extension and pathogenicity assays.
  • Green fluorescent protein (GFP) fusion protein localization and fluorescence microscopy.
  • Electron microscopy to examine hyphal tip ultrastructure.

Main Results:

  • Two kinesin genes, kin1 and kin2, were identified. Kin1 deletion showed no phenotype, while kin2 deletion severely impaired hyphal extension and pathogenicity.
  • Wild-type dikaryons exhibited rapid tip growth with directed cytoplasmic flow, whereas delta kin2 mutants had short, cytoplasm-filled hyphae.
  • GFP-Kin2 localized to hyphal tips, and electron microscopy revealed vesicle accumulation at wild-type hyphal tips, absent in mutants.

Conclusions:

  • The kinesin motor protein Kin2 is crucial for Ustilago maydis filamentous growth and pathogenicity.
  • Kin2 likely organizes the hyphal tip growth zone by regulating vectorial vesicle transport.

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