Modulation of activity of Bacillus subtilis regulatory proteins GltC and TnrA by glutamate dehydrogenase
Modulation of activity of Bacillus subtilis regulatory proteins GltC and TnrA by glutamate dehydrogenase
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DOI：
10.1128/jb.186.11.3399-3407.2004
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发表时间：
2004-06-01
影响因子：
3.2
通讯作者：
Sonenshein, AL
中科院分区：
文献类型：
--
作者：
Belitsky, BR;Sonenshein, AL
编码谷氨酸合酶的枯草芽孢杆菌 gltAB 操纵子需要特定的正调节因子 GltC 来表达，并受到全局调节蛋白 TnrA 的抑制。控制 TnrA 活性的因子（谷氨酰胺合成酶和反馈抑制剂（例如谷氨酰胺）的复合物）是已知的，但调节 GltC 活性的信号仍然难以捉摸。当细胞在含有精氨酸、鸟氨酸或脯氨酸的培养基中生长时，GltC 依赖性 gltAB 表达急剧减少，所有这些都是 Roc 分解代谢途径的诱导剂和底物。对Roc途径中存在各种缺陷的突变体中gltAB表达的分析表明，这种抑制需要rocG编码的谷氨酸脱氢酶，这表明该酶的底物或产物是GltC的真正效应子。鉴于 RocG 是谷氨酸分解代谢的酶，GltC 的主要调节作用可能是在精氨酸相关氨基酸或脯氨酸存在的情况下防止谷氨酸合成和降解的无效循环。此外，谷氨酸脱氢酶的高活性与TnrA的活性不相容。
The Bacillus subtilis gltAB operon, encoding glutamate synthase, requires a specific positive regulator, GltC, for its expression and is repressed by the global regulatory protein TnrA. The factor that controls TnrA activity, a complex of glutamine synthetase and a feedback inhibitor, such as glutamine, is known, but the signal for modulation of GltC activity has remained elusive. GltC-dependent gltAB expression was drastically reduced when cells were grown in media containing arginine or ornithine or proline, all of which are inducers and substrates of the Roc catabolic pathway. Analysis of gltAB expression in mutants with various defects in the Roc pathway indicated that rocG-encoded glutamate dehydrogenase was required for such repression, suggesting that the substrates or products of this enzyme are the real effectors of GltC. Given that RocG is an enzyme of glutamate catabolism, the main regulatory role of GltC may be prevention of a futile cycle of glutamate synthesis and degradation in the presence of arginine-related amino acids or proline. In addition, high activity of glutamate dehydrogenase was incompatible with activity of TnrA.