缺乏S-腺苷甲硫氨酸会导致大肠杆菌出现细胞分裂缺陷。
Lack of S-adenosylmethionine results in a cell division defect in Escherichia coli.
作者信息
Newman E B, Budman L I, Chan E C, Greene R C, Lin R T, Woldringh C L, D'Ari R
机构信息
Biology Department, Concordia University Montreal, Quebec H3G 1M8.
出版信息
J Bacteriol. 1998 Jul;180(14):3614-9. doi: 10.1128/JB.180.14.3614-3619.1998.
Abstract
The enzyme S-adenosylmethionine (SAM) synthetase, the Escherichia coli metK gene product, produces SAM, the cell's major methyl donor. We show here that SAM synthetase activity is induced by leucine and repressed by Lrp, the leucine-responsive regulatory protein. When SAM synthetase activity falls below a certain critical threshold, the cells produce long filaments with regularly distributed nucleoids. Expression of a plasmid-carried metK gene prevents filamentation and restores normal growth to the metK mutant. This indicates that lack of SAM results in a division defect.
摘要
酶S-腺苷甲硫氨酸（SAM）合成酶是大肠杆菌metK基因的产物，可产生SAM，即细胞的主要甲基供体。我们在此表明，SAM合成酶活性受亮氨酸诱导，并受亮氨酸响应调节蛋白Lrp抑制。当SAM合成酶活性降至某个临界阈值以下时，细胞会产生带有规则分布类核的长丝。携带质粒的metK基因的表达可防止丝化，并使metK突变体恢复正常生长。这表明SAM的缺乏会导致分裂缺陷。
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