Kapatral Vinayak, Campbell John W, Minnich Scott A, Thomson Nicholas R, Matsumura Philip, Prüß Birgit M
Integrated Genomics, Inc., 2201 West Campbell Park Dr., Chicago, IL 60612, USA.
Department of Microbiology, Molecular Biology and Biochemistry, University of Idaho, Moscow, ID 83843, USA.
Microbiology (Reading). 2004 Jul;150(Pt 7):2289-2300. doi: 10.1099/mic.0.26814-0.
This paper focuses on global gene regulation by FlhD/FlhC in enteric bacteria. Even though Yersinia enterocolitica FlhD/FlhC can complement an Escherichia coli flhDC mutant for motility, it is not known if the Y. enterocolitica FlhD/FlhC complex has an effect on metabolism similar to E. coli. To study metabolic gene regulation, a partial Yersinia enterocolitica 8081c microarray was constructed and the expression patterns of wild-type cells were compared to an flhDC mutant strain at 25 and 37 degrees C. The overlap between the E. coli and Y. enterocolitica FlhD/FlhC regulated genes was 25 %. Genes that were regulated at least fivefold by FlhD/FlhC in Y. enterocolitica are genes encoding urocanate hydratase (hutU), imidazolone propionase (hutI), carbamoylphosphate synthetase (carAB) and aspartate carbamoyltransferase (pyrBI). These enzymes are part of a pathway that is involved in the degradation of L-histidine to L-glutamate and eventually leads into purine/pyrimidine biosynthesis via carbamoylphosphate and carbamoylaspartate. A number of other genes were regulated at a lower rate. In two additional experiments, the expression of wild-type cells grown at 4 or 25 degrees C was compared to the same strain grown at 37 degrees C. The expression of the flagella master operon flhD was not affected by temperature, whereas the flagella-specific sigma factor fliA was highly expressed at 25 degrees C and reduced at 4 and 37 degrees C. Several other flagella genes, all of which are under the control of FliA, exhibited a similar temperature profile. These data are consistent with the hypothesis that temperature regulation of flagella genes might be mediated by the flagella-specific sigma factor FliA and not the flagella master regulator FlhD/FlhC.
本文聚焦于肠道细菌中FlhD/FlhC对全局基因的调控。尽管小肠结肠炎耶尔森菌的FlhD/FlhC能够互补大肠杆菌flhDC突变体的运动能力,但尚不清楚小肠结肠炎耶尔森菌的FlhD/FlhC复合物是否具有与大肠杆菌类似的对代谢的影响。为了研究代谢基因调控,构建了部分小肠结肠炎耶尔森菌8081c微阵列,并比较了野生型细胞与flhDC突变株在25℃和37℃下的表达模式。大肠杆菌和小肠结肠炎耶尔森菌中受FlhD/FlhC调控的基因重叠率为25%。在小肠结肠炎耶尔森菌中受FlhD/FlhC至少五倍调控的基因包括编码尿刊酸水合酶(hutU)、咪唑啉丙酸酶(hutI)、氨甲酰磷酸合成酶(carAB)和天冬氨酸氨甲酰转移酶(pyrBI)的基因。这些酶是参与将L-组氨酸降解为L-谷氨酸的途径的一部分,并最终通过氨甲酰磷酸和氨甲酰天冬氨酸进入嘌呤/嘧啶生物合成。其他一些基因的调控率较低。在另外两个实验中,比较了在4℃或25℃下生长的野生型细胞与在37℃下生长的同一菌株的表达情况。鞭毛主操纵子flhD的表达不受温度影响,而鞭毛特异性σ因子fliA在25℃时高表达,在4℃和37℃时降低。其他几个均受FliA控制的鞭毛基因也表现出类似的温度分布。这些数据与以下假设一致,即鞭毛基因的温度调控可能由鞭毛特异性σ因子FliA介导,而非鞭毛主调节因子FlhD/FlhC。