Stock J, Borczuk A, Chiou F, Burchenal J E
Proc Natl Acad Sci U S A. 1985 Dec;82(24):8364-8. doi: 10.1073/pnas.82.24.8364.
During bacterial chemotaxis membrane receptor proteins are methylated and demethylated at glutamate residues. The generally accepted view is that these reactions play an essential role in the chemosensing mechanism. Strains may be isolated, however, that exhibit chemotaxis in the complete absence of methylation. These are readily obtained by selecting for chemotactic variants of a mutant that completely lacks the methylating enzyme. Methyltransferase activity is not restored; instead, the sensory-motor apparatus is genetically restructured to compensate for the methylation defect. Genetic and biochemical analyses show that the compensatory mutational locus is the structural gene for the demethylating enzyme. Thus, although mutants lacking either the methylating or demethylating enzymes are nonchemotactic, strains defective in both activities exhibit almost-wild-type chemotactic ability.
在细菌趋化作用中，膜受体蛋白在谷氨酸残基处发生甲基化和去甲基化。普遍接受的观点是，这些反应在化学传感机制中起着至关重要的作用。然而，可以分离出在完全没有甲基化的情况下仍表现出趋化作用的菌株。通过选择完全缺乏甲基化酶的突变体的趋化变体很容易获得这些菌株。甲基转移酶活性并未恢复；相反，感觉运动装置在基因上进行了重组以补偿甲基化缺陷。遗传和生化分析表明，补偿性突变位点是去甲基化酶的结构基因。因此，尽管缺乏甲基化酶或去甲基化酶的突变体没有趋化性，但在这两种活性上有缺陷的菌株表现出几乎野生型的趋化能力。
