Abstract
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.
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