Cohn M S, Tabor C W, Tabor H
J Bacteriol. 1980 Jun;142(3):791-9. doi: 10.1128/jb.142.3.791-799.1980.
We isolated several strains of Saccharomyces cerevisiae containing mutations mapping at a single chromosomal gene (spe10); these strains are defective in the decarboxylation of L-ornithine to form putrescine and consequently do not synthesize spermidine and spermine. The growth of one of these mutants was completely eliminated in a polyamine-deficient medium; the growth rate was restored to normal if putrescine, spermidine, or spermine was added. spe10 is not linked to spe2 (adenosylmethionine decarboxylase) or spe3 (putrescine aminopropyltransferase [spermidine synthease]). spe 10 is probably a regulatory gene rather than the structural gene for ornithine decarboxylase, since we isolated two different mutations which bypassed spe10 mutants; these were spe4, an unliked recessive mutation, and spe40, a dominant mutation linked to spe10. Both spe4 and spe40 mutants exhibited a deficiency of spermidine aminopropyltransferase (spermine synthase), but not of putrescine aminopropyltransferase. This suggests that ornithine decarboxylase activity is negatively controlled by the presence of spermidine aminopropyltransferase.
我们分离出了几株酿酒酵母菌株，这些菌株含有位于单个染色体基因（spe10）上的突变；这些菌株在将L-鸟氨酸脱羧形成腐胺的过程中存在缺陷，因此无法合成亚精胺和精胺。其中一个突变体在缺乏多胺的培养基中生长完全被抑制；如果添加腐胺、亚精胺或精胺，生长速率可恢复正常。spe10与spe2（腺苷甲硫氨酸脱羧酶）或spe3（腐胺氨基丙基转移酶[亚精胺合成酶]）不连锁。spe10可能是一个调控基因，而不是鸟氨酸脱羧酶的结构基因，因为我们分离出了两个绕过spe10突变体的不同突变；它们是spe4，一个不连锁的隐性突变，以及spe40，一个与spe10连锁的显性突变。spe4和spe40突变体均表现出亚精胺氨基丙基转移酶（精胺合成酶）缺乏，但腐胺氨基丙基转移酶不缺乏。这表明鸟氨酸脱羧酶活性受到亚精胺氨基丙基转移酶的负调控。
