缺乏NhaA和NhaB蛋白的大肠杆菌突变体的Na⁺和K⁺转运缺陷明显，且是由渗透调节受损所致。
The Na+ and K+ transport deficiency of an E. coli mutant lacking the NhaA and NhaB proteins is apparent and caused by impaired osmoregulation.
作者信息
Verkhovskaya M L, Barquera B, Verkhovsky M I, Wikström M
机构信息
Department of Medical Chemistry, Institute of Biomedical Sciences, University of Helsinki, Finland.
出版信息
FEBS Lett. 1998 Nov 20;439(3):271-4. doi: 10.1016/s0014-5793(98)01380-5.
Cells of the E. coli mutant EP432, which lacks the two Na+/H+ antiporters, NhaA and NhaB, have been reported to have an impaired sodium transport activity (Harel-Bronstein et al. (1995) J. Biol. Chem. 270, 3816-3822). Here we report that active transport of Na+ in EP432 cells can be restored to wild-type levels, either by a high K+ concentration or by an increase in the medium osmolarity. We suggest that this mutant is primarily deficient in osmoregulation rather than in cation transport per se.
据报道，缺乏两种Na⁺/H⁺反向转运蛋白NhaA和NhaB的大肠杆菌突变体EP432的细胞，其钠转运活性受损（哈雷尔 - 布朗斯坦等人，（1995年）《生物化学杂志》270卷，3816 - 3822页）。在此我们报告，通过高钾浓度或培养基渗透压的增加，EP432细胞中Na⁺的主动转运可以恢复到野生型水平。我们认为，该突变体主要在渗透调节方面存在缺陷，而非阳离子转运本身存在缺陷。
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