Yamamoto Kaneyoshi, Matsumoto Fumika, Minagawa Shu, Oshima Taku, Fujita Nobuyuki, Ogasawara Naotake, Ishihama Akira
Department of Frontier Bioscience and Research Center for Micro-Nano Technology, Hosei University, Koganei, Tokyo, Japan.
Biosci Biotechnol Biochem. 2009 Feb;73(2):346-50. doi: 10.1271/bbb.80586. Epub 2009 Feb 7.
In Escherichia coli, CitA is a membrane-associated sensor histidine kinase that phosphorylates CitB, the response regulator. It is predicated to play a key role in anaerobic citrate catabolism. The citrate-binding site in CitA is located within its periplasmic domain, while the cytoplasmic domain (CitA-C) is involved in autophosphorylation. We found that autophosphorylation in vitro of CitA-C was induced by DTT. Using the whole set of CitA-C derivatives containing Cys-Ala substitution(s), Cys at 529 was found to be essential to the redox-sensing of autophosphorylation. The phosphorylated CitA-C transferred a phosphate to CitB. DNase-I footprinting assay indicated that CitB specifically bound on the intergenic region between the citA and citC genes. These results characterize the molecular mechanism of the CitA-CitB signal transduction system in E. coli.
在大肠杆菌中,CitA是一种与膜相关的传感组氨酸激酶,可使响应调节因子CitB磷酸化。据推测,它在厌氧柠檬酸盐分解代谢中起关键作用。CitA中的柠檬酸盐结合位点位于其周质结构域内,而细胞质结构域(CitA-C)参与自磷酸化。我们发现,DTT可诱导CitA-C在体外进行自磷酸化。使用包含半胱氨酸-丙氨酸取代的整套CitA-C衍生物,发现529位的半胱氨酸对于自磷酸化的氧化还原传感至关重要。磷酸化的CitA-C将磷酸基团转移至CitB。DNase-I足迹分析表明,CitB特异性结合在citA和citC基因之间的基因间区域。这些结果表征了大肠杆菌中CitA-CitB信号转导系统的分子机制。