Abstract

Farnesol was the first quorum-sensing regulator to be found in eukaryotic cells. In Candida albicans, a dimorphic fungal human pathogen, farnesol blocks the yeast-to-filamentous growth transition. Here we show that in Aspergillus niger farnesol acts as an inhibitor of conidiation: Colonies grown on media containing farnesol were unable to develop conidia. Although farnesol treated A. niger cultures exhibited a colony morphology resembling the "fluffy" phenotype of A. nidulans, which is caused by a hyperactive G-protein/cAMP pathway, the intracellular level of cAMP in A. niger mycelia grown in presence of farnesol is greatly diminished. Furthermore, whereas inhibiting adenylyl cyclase led to a farnesol-like effect, the addition of external cAMP inhibited conidiation without causing a "fluffy" phenotype. This suggests that the mechanisms regulating conidiation in A. niger and A. nidulans are different.

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