Biology Department, Concordia University, 1455 de Maisonneuve Ave., Montreal, Quebec H3G 1M8, Canada.
Microbiology (Reading). 2013 Oct;159(Pt 10):2036-2048. doi: 10.1099/mic.0.069682-0. Epub 2013 Aug 2.
An E. coli K-12 mutant deficient in S-adenosylmethionine (SAM) synthesis, i.e ΔmetK, but expressing a rickettsial SAM transporter, can grow in glucose minimal medium if provided with both SAM and methionine. It uses the externally provided (R)-enantiomer of SAM as methyl donor to produce most but not all of its methionine, by methylation of homocysteine catalysed by homocysteine methyltransferase (MmuM). The ΔmetK cells are also altered in growth and are twice as long as those of the parent strain. When starved of SAM, the mutant makes a small proportion of very long cells suggesting a role of SAM and of methylation in the onset of crosswall formation.
一株埃希氏大肠杆菌 K-12 突变株，其 S-腺苷甲硫氨酸（SAM）合成缺陷，即 ΔmetK，但表达了一种立克次氏体 SAM 转运蛋白，如果同时提供 SAM 和蛋氨酸，它可以在葡萄糖最低培养基中生长。它使用外部提供的（R）-SAM 作为甲基供体，通过同型半胱氨酸甲基转移酶（MmuM）催化的同型半胱氨酸甲基化，产生大部分但不是全部的蛋氨酸。ΔmetK 细胞的生长也发生了改变，比亲本菌株长两倍。当 SAM 饥饿时，突变株产生一小部分非常长的细胞，这表明 SAM 和甲基化在细胞壁形成开始时起作用。
