Smith M R
J Bacteriol. 1983 Nov;156(2):516-23. doi: 10.1128/jb.156.2.516-523.1983.
2-Bromoethanesulfonate (BES) inhibition of methanogenesis from methanol by resting-cell suspensions or cell extracts of Methanosarcina was reversed by coenzyme M. BES inhibition of methylcoenzyme M methylreductase activity in cell-free extracts was reversed by methylcoenzyme M but not by coenzyme M. Methanol/coenzyme M methyltransferase activity was not inhibited by 10 microM BES. Inhibition of methylreductase by BES and 3-bromopropionate was competitive with methylcoenzyme M, but inhibition by 2-bromoethanol exhibited mixed kinetics. The Ki values for the inhibitors in cell-free extracts were similar to the concentrations which inhibited intact cells. BES-resistant mutants of strain 227 were apparently permeability mutants because in vitro assays showed that mutant and parent strain methylreductases were equally sensitive to BES.
2-溴乙烷磺酸盐(BES)对静止细胞悬液或甲烷八叠球菌细胞提取物由甲醇生成甲烷的抑制作用可被辅酶M逆转。BES对无细胞提取物中甲基辅酶M甲基还原酶活性的抑制作用可被甲基辅酶M逆转,但不能被辅酶M逆转。甲醇/辅酶M甲基转移酶活性不受10微摩尔BES的抑制。BES和3-溴丙酸对甲基还原酶的抑制作用与甲基辅酶M具有竞争性,但2-溴乙醇的抑制作用表现出混合动力学。无细胞提取物中抑制剂的Ki值与抑制完整细胞的浓度相似。227菌株的BES抗性突变体显然是通透性突变体,因为体外试验表明突变体和亲本菌株的甲基还原酶对BES的敏感性相同。