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This study explores signal transduction pathways that function during mating and infection in the opportunistic, human fungal pathogen Cryptococcus neoformans.  The gene encoding a G-protein α subunit homolog,  GPA1,  was disrupted by homologous recombination. The  gpa1  mutant strain was viable but exhibited a defect in mating in response to nitrogen starvation. Additionally, the  gpa1  mutant strain failed to induce two well-established virulence factors—melanin synthesis, in response to glucose starvation; and capsule production, in response to iron limitation. As a consequence, virulence of the  gpa1  mutant strain was significantly attenuated in an animal model of cryptococcal meningitis. Reintroduction of the wild-type  GPA1  gene complemented the gpa1  mutant phenotypes and restored mating, melanin and capsule production, and virulence. Similarly, exogenous cAMP also suppressed the  gpa1  mutant phenotypes, restoring mating and production of melanin and capsule. These observations support a model in which GPA1 has a role in sensing diverse environmental signals required for mating and virulence by regulating cAMP metabolism in  C. neoformans.

Cryptococcus neoformans mating and virulence are regulated by the G-protein α subunit GPA1 and cAMP