Different signalling pathways involving a Gα protein, cAMP and a MAP kinase control germination of Botrytis cinerea conidia

Conidial germination of the grey mould fungus Botrytis cinerea was found to be induced by different chemical and physical signals, namely the amount and quality of nutrients as well as the hydrophobicity and rigidity of the surface. A B. cinerea Delta bcg3 mutant disrupted in the G alpha 3 subunit of the heterotrimeric G protein was specifically defective in germination induced by carbon sources. A similar germination defect of an adenylate cyclase mutant, and the complementing effect of cAMP addition to conidia of these mutants confirmed the involvement of cAMP. In contrast, a Delta bmp1 MAP kinase mutant was delayed in carbon source-induced germination, but completely unable to germinate on hydrophobic surfaces. Based on these data, it is proposed that the germination response of B. cinerea conidia is controlled by three signalling pathways: Germination induction by rich media is weakly dependent on BMP1; induction by carbon sources requires BCG3, cAMP and BMP1; and induction by contact to hydrophobic surfaces is absolutely dependent on BMP1. Other defects of the Delta bcg3 mutant, such as low conidiation, excessive formation of sclerotia and delayed host infection, were also restored by cAMP. Microscopical studies of germling growth and differentiation on host cuticles revealed that the delayed infection of the Delta bcg3 mutant was due to a surface sensing defect leading to a reduced penetration. Thus, in addition to their role in germination, G alpha 3, cAMP as well as BMP1 are required also for proper host surface recognition and penetration ability of germinated conidia.