Allen E R, Orrego C, Wabiko H, Freese E
J Bacteriol. 1986 Apr;166(1):1-8. doi: 10.1128/jb.166.1.1-8.1986.
In contrast to Escherichia coli and Salmonella typhimurium, Bacillus subtilis could convert ethionine to S-adenosylethionine (SAE), as can Saccharomyces cerevisiae. This conversion was essential for growth inhibition by ethionine because metE mutants which were deficient in S-adenosylmethionine synthetase activity, were resistant to 10 mM ethionine and converted only a small amount of ethionine to SAE. Another mutation (ethA1) produced partial resistance to ethionine (2 mM) and enabled continual sporulation in glucose medium containing 4 mM DL-ethionine. This sporulation induction probably resulted from the effect of SAE, since it was abolished by the addition of a metE1 mutation. The induction of sporulation was not simply controlled by the ratio of SAE to S-adenosylmethionine, but apparently depended on another effect of the ethA1 mutation, which could be demonstrated by comparing the restriction of clear plaque mutants of bacteriophage phi 105 grown in an ethA1 strain with the restriction of those grown in the standard strain. The phages grown in the ethA1 strain showed increased protection against BsuR restriction. We propose that SAE induces sporulation through the inhibition of a key methylation reaction.
与大肠杆菌和鼠伤寒沙门氏菌不同，枯草芽孢杆菌能够将乙硫氨酸转化为S -腺苷乙硫氨酸（SAE），酿酒酵母也能如此。这种转化对于乙硫氨酸抑制生长至关重要，因为缺乏S -腺苷甲硫氨酸合成酶活性的metE突变体对10 mM乙硫氨酸具有抗性，并且仅将少量乙硫氨酸转化为SAE。另一个突变（ethA1）产生了对乙硫氨酸（2 mM）的部分抗性，并使得在含有4 mM DL -乙硫氨酸的葡萄糖培养基中能够持续产孢。这种产孢诱导可能是由SAE的作用导致的，因为添加metE1突变后这种诱导作用就消失了。产孢诱导并非简单地由SAE与S -腺苷甲硫氨酸的比例控制，而是显然取决于ethA1突变的另一种效应，这可以通过比较在ethA1菌株中生长的噬菌体phi 105的清晰噬菌斑突变体受到的限制与在标准菌株中生长的噬菌体受到的限制来证明。在ethA1菌株中生长的噬菌体对BsuR限制的抗性增强。我们提出SAE通过抑制关键的甲基化反应来诱导产孢。
