Grogan D W
Department of Microbiology, University of Illinois, Urbana 61801.
Arch Microbiol. 1988;150(4):363-7. doi: 10.1007/BF00408308.
The basis for disruption of morphogenesis by depletion of pyridoxine derivatives was studied using a pdxH null mutant of Escherichia coli K-12. Removal of pyridoxal from growing cultures severely inhibited murein synthesis in vivo, whereas simultaneous supplementation with D-alanine effectively prevented inhibition. Extractable alanine racemase was low following such starvation. Selection of mutants overcoming the glycine- or temperature-sensitivity imposed by pyridoxine limitation yielded a variety of phenotypes. The most effective of these extragenic suppressors conferred an elevated alanine racemase activity which was resistant to the effects of pyridoxal removal.
利用大肠杆菌K-12的pdxH基因缺失突变体，研究了吡哆醇衍生物缺乏导致形态发生破坏的基础。从正在生长的培养物中去除吡哆醛会严重抑制体内胞壁质的合成，而同时补充D-丙氨酸可有效防止抑制作用。在这种饥饿状态下，可提取的丙氨酸消旋酶含量较低。筛选克服吡哆醇限制所导致的甘氨酸敏感性或温度敏感性的突变体，产生了多种表型。这些基因外抑制子中最有效的一种可使丙氨酸消旋酶活性升高，且该活性对去除吡哆醛的影响具有抗性。
