Reoyo E, Espeso E A, Peñalva M A, Suárez T
Departamento de Microbiología Molecular, Centro de Investigaciones Biológicas (C.S.I.C.), Velázquez, Madrid, Spain.
Fungal Genet Biol. 1998 Apr;23(3):288-99. doi: 10.1006/fgbi.1998.1039.
pmaA, an Aspergillus nidulans gene encoding a P-ATPase, has been cloned by heterologous hybridization with the yeast PMA1 gene. The putative 990-residue PmaA polypeptide shows 50% identity to Saccharomyces cerevisiae and Neurospora crassa plasma membrane H(+)-ATPases and weak (19-26%) identity to other yeast P-type cation-translocating ATPases. PmaA contains all catalytic domains characterizing H(+)-ATPases. pmaA transcript levels are not regulated by PacC, the transcription factor mediating pH regulation, and were not significantly affected by an extreme creAd mutation resulting in carbon catabolite derepression. Deletion of pmaA causes lethality, but a single copy of the gene is sufficient to support normal growth rate in pmaA hemizygous diploids, even under acidic growth conditions. As compared to other fungal H(+)-ATPases, PmaA presents three insertions, 39, 7, and 16 residues long, in the conserved central region of the protein. Two of these insertions are predicted to be located in extracellular loops and might be of diagnostic value for the identification of Aspergillus species. Their absence from most mammalian P-type ATPases may have implications for antifungal therapy.
pmaA是构巢曲霉中一个编码P型ATP酶的基因，通过与酵母PMA1基因进行异源杂交而被克隆。推测的由990个氨基酸残基组成的PmaA多肽与酿酒酵母和粗糙脉孢菌的质膜H⁺-ATP酶有50%的同源性，与其他酵母P型阳离子转运ATP酶有较弱的同源性（19%-26%）。PmaA含有所有表征H⁺-ATP酶的催化结构域。pmaA转录水平不受PacC（介导pH调节的转录因子）调控，并且不受导致碳分解代谢物阻遏解除的极端creA⁻突变的显著影响。pmaA的缺失会导致致死性，但该基因的单拷贝足以支持pmaA半合子二倍体的正常生长速率，即使在酸性生长条件下也是如此。与其他真菌H⁺-ATP酶相比，PmaA在该蛋白质保守的中央区域有三个插入片段，分别为39、7和16个氨基酸残基长。其中两个插入片段预计位于细胞外环中，可能对构巢曲霉属物种的鉴定具有诊断价值。大多数哺乳动物P型ATP酶中没有这些插入片段，这可能对抗真菌治疗有影响。
