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Journal of Bacteriology, November 2005, p. 7647-7654, Vol. 187, No. 22
0021-9193/05/$08.00+0     doi:10.1128/JB.187.22.7647-7654.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Stabilization of Polar Localization of a Chemoreceptor via Its Covalent Modifications and Its Communication with a Different Chemoreceptor

Daisuke Shiomi,1,{dagger} Satomi Banno,1 Michio Homma,1 and Ikuro Kawagishi1,2*

Division of Biological Science, Graduate School of Science,1 Institute for Advanced Research, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan2

Received 12 January 2005/ Accepted 26 July 2005

In the chemotaxis of Escherichia coli, polar clustering of the chemoreceptors, the histidine kinase CheA, and the adaptor protein CheW is thought to be involved in signal amplification and adaptation. However, the mechanism that leads to the polar localization of the receptor is still largely unknown. In this study, we examined the effect of receptor covalent modification on the polar localization of the aspartate chemoreceptor Tar fused to green fluorescent protein (GFP). Amidation (and presumably methylation) of Tar-GFP enhanced its own polar localization, although the effect was small. The slight but significant effect of amidation on receptor localization was reinforced by the fact that localization of a noncatalytic mutant version of GFP-CheR that targets to the C-terminal pentapeptide sequence of Tar was similarly facilitated by receptor amidation. Polar localization of the demethylated version of Tar-GFP was also enhanced by increasing levels of the serine chemoreceptor Tsr. The effect of covalent modification on receptor localization by itself may be too small to account for chemotactic adaptation, but receptor modification is suggested to contribute to the molecular assembly of the chemoreceptor/histidine kinase array at a cell pole, presumably by stabilizing the receptor dimer-to-dimer interaction.

* Corresponding author. Mailing address: Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan. Phone: 81 52 789 2993. Fax: 81 52 789 3001. E-mail: i45406a{at}cc.nagoya-u.ac.jp.

{dagger} Present address: Microbiology and Molecular Genetics, University of Texas Medical School, Houston, TX 77030.

Journal of Bacteriology, November 2005, p. 7647-7654, Vol. 187, No. 22
0021-9193/05/$08.00+0     doi:10.1128/JB.187.22.7647-7654.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Irieda, H., Homma, M., Homma, M., Kawagishi, I. (2006). Control of Chemotactic Signal Gain via Modulation of a Pre-formed Receptor Array. J. Biol. Chem. 281: 23880-23886 [Abstract] [Full Text]  
  • Ward, S. M., Bormans, A. F., Manson, M. D. (2006). Mutationally Altered Signal Output in the Nart (NarX-Tar) Hybrid Chemoreceptor. J. Bacteriol. 188: 3944-3951 [Abstract] [Full Text]  


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