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首页> 外文期刊>Journal of bacteriology >Influence of methionine biosynthesis on serine transhydroxymethylase regulation in Salmonella typhimurium LT2.
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Influence of methionine biosynthesis on serine transhydroxymethylase regulation in Salmonella typhimurium LT2.

机译：蛋氨酸生物合成对鼠伤寒沙门氏菌LT2中丝氨酸羟甲基化酶调控的影响。

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摘要

The enzyme serine transhydroxymethylase (EC 2.1.2.1; L-serine:tetrahydrofolate-5,10-hydroxymethyltransferase) is responsible both for the synthesis of glycine from serine and production of the 5,10-methylenetetrahydrofolate necessary as a methyl donor for methionine synthesis. Two mutants selected for alteration in serine transhydroxymethylase regulation also have phenotypes characteristic of metK (methionine regulatory) mutants, including ethionine, norleucine, and alpha-methylmethionine resistance and reduced levels of S-adenosylmethionine synthetase (EC 2.5.1.6; adenosine 5'-triphosphate:L-methionine S-adenosyltransferase) activity. Because this suggested the existence of a common regulatory component, the regulation of serine transhydroxymethylase was examined in other methionine regulatory mutants (metK and metJ mutants). Normally, serine transhydroxymethylase levels are repressed three- to sixfold in cells grown in the presence of serine, glycine, methionine, adenine, guanine, and thymine. This does not occur in metK and metJ mutants; thus, these mutations do affect the regulation of both serine transhydroxymethylase and the methionine biosynthetic enzymes. Lesions in the metK gene have been reported to reduce S-adenosylmethionine synthetase levels. To determine whether the metK gene actually encodes for S-adenosylmethionine synthetase, a mutant was characterized in which this enzyme has a 26-fold increased apparent Km for methionine. This mutation causes a phenotype associated with metK mutants and is cotransducible with the serA locus at the same frequency as metK lesions. Thus, the affect of metK mutations on the regulation of glycine and methionine synthesis in Salmonella typhimurium appears to be due to either an altered S-adenosylmethionine synthetase or altered S-adenosylmethionine pools.
机译：丝氨酸转羟甲基化酶（EC 2.1.2.1; L-丝氨酸：四氢叶酸-5,10-羟甲基转移酶）既负责由丝氨酸合成甘氨酸，又负责生产作为蛋氨酸合成的甲基供体所必需的5,10-亚甲基四氢叶酸。选择用于改变丝氨酸羟甲基化酶调节作用的两个突变体也具有metK（蛋氨酸调节）突变体的表型，包括乙硫氨酸，正亮氨酸和α-甲基甲硫氨酸抗性，以及S-腺苷甲硫氨酸合成酶水平降低（EC 2.5.1.6;腺苷5'-三磷酸酯） ：L-蛋氨酸S-腺苷转移酶）活性。因为这表明存在共同的调节成分，所以在其他蛋氨酸调节突变体（metK和metJ突变体）中检查了丝氨酸转羟甲基化酶的调节。通常，在存在丝氨酸，甘氨酸，蛋氨酸，腺嘌呤，鸟嘌呤和胸腺嘧啶的情况下生长的细胞中，丝氨酸转羟甲基化酶的水平会降低三到六倍。在metK和metJ突变体中不会发生这种情况;因此，这些突变确实影响丝氨酸转羟甲基酶和蛋氨酸生物合成酶的调节。据报道，metK基因中的病变可降低S-腺苷甲硫氨酸合成酶的水平。为了确定metK基因是否真正编码S-腺苷甲硫氨酸合成酶，表征了一个突变体，其中该酶的甲硫氨酸表观Km增加了26倍。该突变导致与metK突变体相关的表型，并且可与serA基因座以与metK损伤相同的频率共转导。因此，metK突变对鼠伤寒沙门氏菌中甘氨酸和蛋氨酸合成调控的影响似乎是由于S-腺苷甲硫氨酸合成酶的改变或S-腺苷甲硫氨酸池的改变。

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