Two zinc finger transcription factors, CrzA and SltA, are involved in cation homoeostasis and detoxification in Aspergillus nidulans

To investigate cation adaptation and homoeostasis in Aspergillus nidulans, two transcription-factor-encoding genes have been characterized. The A. nidulans orthologue crzA of the Saccharomyces cerevisiae CRZI gene, encoding a transcription factor mediating gene regulation by Ca2+, has been identified and deleted. The crzA deletion phenotype includes extreme sensitivity to alkaline pH, Ca2+ toxicity and aberrant morphology connected with alterations of cell-wall-related phenotypes Such as reduced expression of a chitin synthase gene, chsB. A fully functional C-terminally GFP (green fluorescent protein)-tagged form of the CrzA protein is apparently excluded from nuclei in the absence of added Ca2+, but rapidly accumulates in nuclei upon exposure to Ca2+. In addition, the previously identified sltA gene, which has no identifiable homologues in yeasts, was deleted, and the resulting phenotype includes considerably enhanced toxicity by a number of cations other than Ca2+ and also by alkaline pH. Reduced expression of a homologue of the S. cerevisiae P-type ATPase Na+ pump gene ENAI might partly explain the cation sensitivity of sltA-null strains. Up-regulation of the homologue of the S. cerevisiae vacuolar Ca2+/H+ exchanger gene VCX1 might explain the lack of Ca2+ toxicity to null-sltA Mutants, whereas down-regulation of this gene might be responsible for Ca2+ toxicity to crzA-null mutants. Both crzA and sltA encode DNA-binding proteins, and the latter exerts both positive and negative gene regulation.