Abstract

The dimorphic switch from budding to filamentous growth is an essential morphogenetic transition many fungi utilize to cause disease in the host. Although different environmental signals can induce filamentous growth, the developmental programs associated with transmitting these different signals may differ. Here, we explore the relationship between filamentation and expression levels of ammonium transporters (AMTs) that also sense low ammonium for Ustilago maydis, the pathogen of maize. Overexpression of the high affinity ammonium transporter, Ump2, under normally non-inducing conditions, results in filamentous growth. Furthermore, ump2 expression levels are correlated with expression of genes involved in the mating response pathway and in pathogenicity. Ump1 and Ump2 transcription levels also tracked expression of genes normally up-regulated during either filamentous growth or during growth of the fungus inside the host. Interestingly, haploid strains deleted for the b mating-type locus, like those deleted for ump2, failed to filament on low ammonium; they also shared some alterations in gene expression patterns with cells deleted for ump2 or over-expressing this gene. Deletion of ump2 either in both mating partners or in a solopathogenic haploid strain resulted in a dramatic reduction in disease severity for infected plants, suggesting some importance of this transceptor in the pathogenesis program.

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