Bassford P J, Bradbeer C, Kadner R J, Schnaitman C A
J Bacteriol. 1976 Oct;128(1):242-7. doi: 10.1128/jb.128.1.242-247.1976.
It is known that the tonB mutation in Escherichia coli is responsible for a defect in the transport of iron chelates. These are transported by systems that involve outer membrane components. We found that tonB mutants were also deficient in the secondary, energy-dependent phase of vitamin B12 transport, although the mutants have normal levels of B12 receptors on their cell surface. In addition, tonB mutants derived from vitamin B12 auxotrophs required elevated levels of B12 for normal growth. Maltose uptake, mediated by another transport system involving an outer membrane component, was unaffected by the tonB mutation.
已知大肠杆菌中的tonB突变会导致铁螯合物转运缺陷。这些铁螯合物通过涉及外膜成分的系统进行转运。我们发现,tonB突变体在维生素B12转运的次级能量依赖阶段也存在缺陷,尽管这些突变体细胞表面的B12受体水平正常。此外,源自维生素B12营养缺陷型的tonB突变体需要更高水平的B12才能正常生长。由另一个涉及外膜成分的转运系统介导的麦芽糖摄取不受tonB突变的影响。