Mutations in the myp1 gene of Ustilago maydis attenuate mycelial growth and virulence.

Abstract

Mating between haploid, budding cells of the dimorphic fungus Ustilago maydis results in the formation of a dikaryotic, filamentous cell type. Mating compatibility is governed by two mating-type loci called a and b; transformation of genes from these loci (e.g. a1 and b1) into a haploid strain of different mating type (e.g. a2 b2) allows filamentous growth and establishes a pathogenic cell type. Several mutants with a nonmycelial colony morphology were isolated after insertional mutagenesis of a filamentous, pathogenic haploid strain. The mutagenized region in one such mutant was recovered by plasmid rescue and employed to isolate a gene involved in conditioning the mycelial phenotype (myp1). An 1150 amino acid open reading frame is present at the myp1 locus; the predicted polypeptide is rich in serine residues and contains short regions with similarity to SH3 domain ligands. Construction of myp1 disruption and deletion mutants in haploid strains confirmed that this gene plays a role in mycelial growth and virulence.