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Gene array analysis of Yersinia enterocolitica FlhD and FlhC: regulation of enzymes affecting synthesis and degradation of carbamoylphosphate

Birgit M. Prüß^4,

¹ Integrated Genomics, Inc., 2201 West Campbell Park Dr., Chicago, IL 60612, USA
² Department of Microbiology, Molecular Biology and Biochemistry, University of Idaho, Moscow, ID 83843, USA
³ The Wellcome Trust Sanger Institute, Genome Campus, Hinxton, Cambridge CB10 1RQ, UK
⁴ Department of Microbiology and Immunology, University of Illinois at Chicago, Chicago, IL 60612-7344, USA

Correspondence
Birgit M. Prüß
preuss{at}uic.edu
or
BirgitPruess{at}ndsu.nodak.edu

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 °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 °C was compared to the same strain grown at 37 °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 °C and reduced at 4 and 37 °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.

Present address: Department of Veterinary and Microbiological Sciences, North Dakota State University, Fargo, ND 58105, USA.

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