具有吡哆醛激酶缺陷的大肠杆菌明显的吡哆醇转运突变体。
Apparent pyridoxine transport mutants of Escherichia coli with pyridoxal kinase deficiency.
作者信息
Yamada R H, Furukawa Y
出版信息
Biochim Biophys Acta. 1980 Aug 4;600(2):581-4. doi: 10.1016/0005-2736(80)90459-9.
By nitrosoguanidine treatment of a vitamin B-6 auxotroph (KG980) of Escherichia coli, mutants were isolated that require for growth markedly higher concentrations of pyridoxine than the parent strain. One of the mutants, strain HN1, exhibited a severely reduced ability to take up extracellular pyridoxine. Besides, cell-free extracts of HN1 showed an extremely low activity to phosphorylate pyridoxine compared to that of KG980. These findings together with other results suggest that phosphorylation of pyridoxine is essential for the concentration uptake of the vitamin.
通过用亚硝基胍处理大肠杆菌的维生素B-6营养缺陷型菌株（KG980），分离出了一些突变体，这些突变体生长所需的吡哆醇浓度明显高于亲本菌株。其中一个突变体HN1菌株摄取细胞外吡哆醇的能力严重下降。此外，与KG980相比，HN1的无细胞提取物将吡哆醇磷酸化的活性极低。这些发现以及其他结果表明，吡哆醇的磷酸化对于该维生素的浓缩摄取至关重要。
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