Negative regulation of the vacuole-mediated resistance to K(+) stress by a novel C2H2 zinc finger transcription factor encoded by aslA in Aspergillus nidulans.

In fungi and plants, vacuoles function as a storage and sequestration vessel for a wide variety of ions and are responsible for cytosolic ion homeostasis and responses to ionic shock. In the filamentous fungus Aspergillus nidulans, however, little is known about the molecular genetic mechanisms of vacuolar biogenesis and function. In the present study, we analyzed the function of the aslA gene (AN5583) encoding a novel C2H2-type zinc finger transcription factor (TF) in relation to K(+) stress resistance, vacuolar morphology, and vacuolar transporters. The mutant lacking aslA showed increased mycelial growth and decreased branching at high K(+) concentrations. Deletion of aslA also caused elevated K(+) stress-inducible expression of the genes, nhxA (AN2288), vnxA (AN6986), and vcxA (AN0471), encoding putative endosomal and vacuolar cation/H(+) exchangers, as well as cpyA and vpsA genes encoding the proteins involved in vacuolar biogenesis. Interestingly, vacuolar fragmentation induced by K(+) stress was alleviated by aslA deletion, resulting in persistence of unfragmented vacuoles. In the presence of bafilomycin, an inhibitor of vacuolar H(+)-ATPase, the mutant phenotype was suppressed in terms of growth rates and vacuolar morphology. These results together suggest that the C2H2-type zinc finger TF AslA attenuates the K(+) stress-inducible expression of the genes encoding the ion pumps involved in vacuolar sequestration of K(+) ions powered by vacuolar H(+)-ATPase, as well as the proteins that function in vacuolar biogenesis.