Figure 7

Tentative model of the mechanistic function of the A. giganteus antifungal protein AFP _NN5353 on Aspergillus sp. The response against AFP_NN5353 attack is mediated via PkcA/MpkA signalling and results in increased agsA transcription. However, the activity of the CWIP occurs independently from RhoA and so far unidentified RhoA-GAP effector molecules might contribute to the AFP_NN5353 toxicity. Furthermore, AFP_NN5353 leads to an immediate and significant increase of the [Ca²⁺]_c resting level in the cell. The sustained perturbation of the Ca²⁺ homeostasis could lead to PCD [17, 34]. The presence of elevated concentrations of extracellular Ca²⁺ counteracts the toxic effects of AFP_NN5353 and improves the resistance of the target organism by decreasing the elevated [Ca²⁺]_c resting level. Whereas cell wall remodelling via CWIP seems to be insufficient to counteract AFP_NN5353 activity, the fortification of the cell wall by the induction of chsD expression might represent an adequate response to increase resistance [15].