Morris D R, Jorstad C M
J Bacteriol. 1970 Mar;101(3):731-7. doi: 10.1128/jb.101.3.731-737.1970.
Mutants defective in the conversion of arginine to putrescine were found by screening clones from mutagenized cultures for inability to produce urea during growth in arginine-supplemented media. Two partially blocked mutants were isolated; one was deficient in arginine decarboxylase and the other was deficient in agmatine ureohydrolase. As predicted from the pattern of putrescine synthesis in Escherichia coli, these mutants were conditionally putrescine-deficient. When grown in either minimal or ornithine-supplemented media, conditions which lead to preferential utilization of the ornithine to putrescine pathway, the mutants had normal intracellular polyamine levels. However, when the mutants were placed in arginine-supplemented media, the level of intracellular putrescine was lowered markedly. Under conditions where intracellular putrescine was 1% of normal, the doubling time of the mutants was increased approximately 10%. The putrescine-deficient mutants had wild-type morphology, normal levels of protein and ribonucleic acid (RNA), and stringent amino acid control of RNA synthesis.
通过筛选诱变培养物中的克隆,以检测其在补充精氨酸的培养基中生长时无法产生尿素的情况,从而发现了在精氨酸向腐胺转化过程中存在缺陷的突变体。分离出了两个部分受阻的突变体;一个缺乏精氨酸脱羧酶,另一个缺乏胍丁胺脲水解酶。正如从大肠杆菌中腐胺合成模式所预测的那样,这些突变体是条件性腐胺缺陷型。当在基本培养基或补充鸟氨酸的培养基中生长时,这些条件会导致优先利用鸟氨酸到腐胺的途径,突变体的细胞内多胺水平正常。然而,当将突变体置于补充精氨酸的培养基中时,细胞内腐胺水平会显著降低。在细胞内腐胺为正常水平1%的条件下,突变体的倍增时间增加了约10%。腐胺缺陷型突变体具有野生型形态、正常水平的蛋白质和核糖核酸(RNA),并且对RNA合成有严格的氨基酸控制。