Role of mating loci and ammonium transporter expression in stressor sensitivity of haploid cells of Ustilago maydis and levels of pathogenicity

Ustilago maydis is a biotrophic pathogen of maize. In order to cause disease in the host, the fungus must undergo a dimorphic switch from yeast-like, budding state to a filamentous state that allows for plant penetration and propagation of the infection. Different environmental cues can induce filamentous growth and some, specifically low nitrogen availability, are essential for mating to occur in nature. In haploid wild type strains of U. maydis, low nitrogen availability also results in a non-infectious filamentous growth response. Mating is governed by the coordinated expression of genes from the mating loci in U. maydis, the a locus and the b locus. The b locus in particular must play an additional role in haploid cells, as deletion of the locus prevents filamentation due to low nitrogen limitation. Previous work found that the U. maydis genome encodes two ammonium transporters (AMTs), Ump1 and Ump2. While deletion of Ump1 does not produce an observable phenotype, deletion of Ump2 in haploids results in the lost of filamentous growth as a response to low nitrogen, similar to what is observed with deletion of the b locus. Overexpression of the high affinity ammonium transporter, Ump2, results in filamentation under non-inducing conditions and can rescue the filamentation defect of the b locus deletion mutant. Preliminary experiments in the lab suggest that the different mutants just mentioned have different susceptibilities to different abiotic stressors. In light of the discovery, we hypothesized that mutations in the b locus specifically might govern this differential stress tolerance; we tested this hypothesis with several stressors. Finally, we examined the role if any, of diffrent b mutants in pathogenicity