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Substitutions in the Periplasmic Domain of Low-Abundance Chemoreceptor Trg That Induce or Reduce Transmembrane Signaling: Kinase Activation and Context Effects

Beel, Bryan D. and Hazelbauer, Gerald L. (2001) Substitutions in the Periplasmic Domain of Low-Abundance Chemoreceptor Trg That Induce or Reduce Transmembrane Signaling: Kinase Activation and Context Effects. Journal of Bacteriology, 183 (2). pp. 671-679. ISSN 0021-9193. doi:10.1128/JB.183.2.671-679.2001.

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We extended characterization of mutational substitutions in the ligand-binding region of Trg, a low-abundance chemoreceptor of Escherichia coli. Previous investigations using patterns of adaptational methylation in vivo led to the suggestion that one class of substitutions made the receptor insensitive, reducing ligand-induced signaling, and another mimicked ligand occupancy, inducing signaling in the absence of ligand. We tested these deductions with in vitro assays of kinase activation and found that insensitive receptors activated the kinase as effectively as wild-type receptors and that induced-signaling receptors exhibited the low level of kinase activation characteristic of occupied receptors. Differential activation by the two mutant classes was not dependent on high-abundance receptors. Cellular context can affect the function of low-abundance receptors. Assays of chemotactic response and adaptational modification in vivo showed that increasing cellular dosage of mutant forms of Trg to a high-abundance level did not significantly alter phenotypes, nor did the presence of high-abundance receptors significantly correct phenotypic defects of reduced-signaling receptors. In contrast, defects of induced-signaling receptors were suppressed by the presence of high-abundance receptors. Grafting the interaction site for the adaptational-modification enzymes to the carboxyl terminus of induced-signaling receptors resulted in a similar suppression of phenotypic defects of induced-signaling receptors, implying that high-abundance receptors could suppress defects in induced-signaling receptors by providing their natural enzyme interaction sites in trans in clusters of suppressing and suppressed receptors. As in the case of cluster-related functional assistance provided by high-abundance receptors for wild-type low-abundance receptors, suppression by high-abundance receptors of phenotypic defects in induced-signaling forms of Trg involved assistance in adaptation, not signaling.

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Additional Information:Copyright © 2001, American Society for Microbiology. Received 5 May 2000/Accepted 26 October 2000 We thank Alexander Barnakov and Ludmilla Barnakova for purified CheA, CheW, CheY, and Trg; Xiuhong Feng for guidance on the kinase assay; Megan Peach for her model of the Trg periplasmic domain; and Douglas Banks and Angela Lilly for introduction of signaling mutations into the hybrid gene coding for Trgt and for initial characterization of those constructs. This work was supported in part by research grant GM29963 and Biotechnology Training Grant T32 GM08336 from the National Institutes of General Medical Science.
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Deposited On:20 Feb 2006
Last Modified:08 Nov 2021 19:42

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