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J Bacteriol, April 1998, p. 1862-1868, Vol. 180, No. 7
Division of Biological Science, Graduate
School of Science, Nagoya University, Chikusa-ku, Nagoya 464-0814, Japan
Received 7 November 1997/Accepted 29 January 1998
In Escherichia coli and Salmonella
typhimurium, methylation and demethylation of receptors are
responsible for chemotactic adaptation and are catalyzed by the
methyltransferase CheR and the methylesterase CheB, respectively. Among
the chemoreceptors of these species, Tsr, Tar, and Tcp have a
well-conserved carboxy-terminal motif (NWET/SF) that is absent in Trg
and Tap. When they are expressed as sole chemoreceptors, Tsr, Tar, and
Tcp support good adaptation, but Trg and Tap are poorly methylated and
supported only weak adaptation. It was recently discovered that CheR
binds to the NWETF sequence of Tsr in vitro. To examine the
physiological significance of this binding, we characterized mutant
receptors in which this pentapeptide sequence was altered.
C-terminally-mutated Tar and Tcp expressed in a receptorless E. coli strain mediated responses to aspartate and citrate,
respectively, but their adaptation abilities were severely impaired.
Their expression levels and attractant-sensing abilities were similar
to those of the wild-type receptors, but the methylation levels of the
mutant receptors increased only slightly upon addition of attractants.
When CheR was overproduced, both the adaptation and methylation
profiles of the mutant Tar receptor became comparable to those of
wild-type Tar. Furthermore, overproduction of CheR also enhanced
adaptive methylation of wild-type Trg, which lacks the NWETF sequence,
in the absence of any other chemoreceptor. These results suggest that
the pentapeptide sequence facilitates effective adaptation and
methylation by recruiting CheR.
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Chemotactic Adaptation Is Altered by Changes in the
Carboxy-Terminal Sequence Conserved among the Major
Methyl-Accepting Chemoreceptors
*
Corresponding author. Mailing address: Division of
Biological Science, Graduate School of Science, Nagoya University,
Chikusa-ku, Nagoya 464-0814, Japan. Phone: 81-52-789-2993. Fax:
81-52-789-3001. E-mail:
i45406a{at}nucc.cc.nagoya-u.ac.jp.
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