Borczuk A, Stock A, Stock J
J Bacteriol. 1987 Jul;169(7):3295-300. doi: 10.1128/jb.169.7.3295-3300.1987.
We previously showed that a mutant strain of Salmonella typhimurium completely deficient in both the chemoreceptor methylating (CheR) and demethylating (CheB) enzymes can still exhibit chemotaxis to aspartate and other attractants (J. Stock, A. Borczuk, F. Chiou, and J. E. B. Burchenal, Proc. Natl. Acad. Sci. USA 82:8364-8368, 1985). We used this cheR cheB mutant to examine the possibility of an additional requirement for S-adenosylmethionine in chemotaxis besides its role in chemoreceptor methylation. A metE mutation was transduced into a cheR cheB double mutant, and the cells were starved for methionine. Despite the fact that intracellular S-adenosylmethionine dropped from approximately 100 microM to less than 0.2 microM, chemotaxis was largely unaffected. In contrast, a corresponding cheR+ cheB+ metE mutant completely lost its chemotaxis ability after being starved for methionine. We conclude from this observation that the primary requirement for S-adenosylmethionine during bacterial chemotaxis is in the methylation of receptor proteins.
我们先前表明，鼠伤寒沙门氏菌的一种突变菌株，其化学感受器甲基化酶（CheR）和去甲基化酶（CheB）均完全缺失，但仍能对天冬氨酸和其他引诱剂表现出趋化性（J. 斯托克、A. 博尔祖克、F. 邱和J. E. B. 伯切纳尔，《美国国家科学院院刊》82:8364 - 8368，1985年）。我们利用这种cheR cheB突变体来研究除了其在化学感受器甲基化中的作用外，趋化作用中对S - 腺苷甲硫氨酸是否还有其他需求。将metE突变导入cheR cheB双突变体中，然后使细胞处于蛋氨酸饥饿状态。尽管细胞内S - 腺苷甲硫氨酸从大约100微摩尔降至低于0.2微摩尔，但趋化作用基本未受影响。相比之下，相应的cheR + cheB + metE突变体在蛋氨酸饥饿后完全丧失了趋化能力。我们从这一观察结果得出结论，细菌趋化作用过程中对S - 腺苷甲硫氨酸的主要需求在于受体蛋白的甲基化。
