Figure 7.

Tentative model of the mechanistic function of the A. giganteus antifungal protein AFPNN5353 on Aspergillus sp. The response against AFPNN5353 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 AFPNN5353 toxicity. Furthermore, AFPNN5353 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 AFPNN5353 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 AFPNN5353 activity, the fortification of the cell wall by the induction of chsD expression might represent an adequate response to increase resistance [15].

Binder et al. BMC Microbiology 2011 11:209   doi:10.1186/1471-2180-11-209
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