活跃的S-腺苷甲硫氨酸脱羧酶基因的存在会加剧在无法合成腐胺、亚精胺和精胺的酿酒酵母突变体中观察到的生长缺陷。
The presence of an active S-adenosylmethionine decarboxylase gene increases the growth defect observed in Saccharomyces cerevisiae mutants unable to synthesize putrescine, spermidine, and spermine.
作者信息
Balasundaram D, Xie Q W, Tabor C W, Tabor H
机构信息
Laboratory of Biochemical Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892.
出版信息
J Bacteriol. 1994 Oct;176(20):6407-9. doi: 10.1128/jb.176.20.6407-6409.1994.
Abstract
Saccharomyces cerevisiae spe1 delta SPE2 mutants (lacking ornithine decarboxylase) and spe1 delta spe2 delta mutants (lacking both ornithine decarboxylase and S-adenosylmethionine decarboxylase) are equally unable to synthesize putrescine, spermidine, and spermine and require spermidine or spermine for growth in amine-free media. The cessation of growth, however, occurs more rapidly in spe1 delta SPE2 cells than in SPE1 spe2 delta or spe1 delta spe2 delta cells. Since spe1 delta SPE2 cells can synthesize decarboxylated adenosylmethionine (dcAdoMet), these data indicate that dcAdoMet may be toxic to amine-deficient cells.
摘要
酿酒酵母spe1ΔSPE2突变体（缺乏鸟氨酸脱羧酶）和spe1Δspe2Δ突变体（既缺乏鸟氨酸脱羧酶又缺乏S-腺苷甲硫氨酸脱羧酶）同样无法合成腐胺、亚精胺和精胺，并且在无胺培养基中生长需要亚精胺或精胺。然而，spe1ΔSPE2细胞中生长停止比在SPE1 spe2Δ或spe1Δspe2Δ细胞中更快。由于spe1ΔSPE2细胞能够合成脱羧腺苷甲硫氨酸（dcAdoMet），这些数据表明dcAdoMet可能对缺乏胺的细胞有毒。
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