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The fungal pathogen Ustilago maydis causes a dramatic disease in maize involving the induction of tumours and the formation of masses of black teliospores. In this fungus, mating between haploid, budding cells results in the formation of the infectious, filamentous cell type that invades host tissue. Mating and filamentous growth are governed by the mating‐type loci and by cAMP signalling, perhaps in response to signals from maize. To dissect the involvement of cAMP signalling further, the constitutive filamentous phenotype of a mutant with a defect in the catalytic subunit of protein kinase A was used to isolate suppressor mutations that restore budding growth. One such mutation identified the hgl1 gene, which is shown to be required for both the switch between budding and filamentous growth and teliospore formation during infection. In addition, the hgl1 gene product may be a target of phosphorylation by protein kinase A, and transcript levels for the gene are elevated during mating. Thus, the hgl1 gene provides a connection between mating, cAMP signalling and two important aspects of virulence: filamentous growth and the formation of teliospores.

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