Fungi rapidly adapt to their environment involving signalling pathways, e.g. those under the control of mitogen activated protein kinases (MAPKs). The fungicide fludioxonil, one of the most efficient fungicides especially against the grey mould agent, Botrytis cinerea, activates the MAPKs involved in osmoregulation, cell wall integrity, development and pathogenicity in this necrotrophic pathogenic fungus. In order to understand the perception and transduction of the fludioxonil signal and, more globally, the stress signalling pathway, a comparative phosphoproteomic analysis using fludioxonil was performed. In a preliminary study approximately hundred differentially phosphorylated proteins were identified in B. cinerea. Among those the phosducin-like protein protein PhnA. Since phosducins are involved in the G-protein signalling pathway, we wanted to understand the involvement of PhnA in fludioxonil signalling and the link to the MAPKs. We have therefore started its functional analysis by gene knock-out. The phnA deletion mutant did not produce necrosis in planta, and displayed reduced in vitro growth. Moreover it has strongly reduced conidia and sclerotia production. Thus phnA is involved in vegetative growth, in development and is a new pathogenicity factor in B. cinerea. We have identified serine 66 in the PhnA protein to be phosphorylated after exposure to fludioxonil. Through the construction of PhnAS66A and PhnAS66D mutants we are currently investigating the role of the phosphorylation status in PhnA function. In addition, the transduction of the fludioxonil signal to the MAPKs Sak1 and Bmp3 will be analysed..