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Attenuation of Sensory Receptor Signaling by Covalent Modification

Borkovich, Katherine A. and Alex, Lisa A. and Simon, Melvin I. (1992) Attenuation of Sensory Receptor Signaling by Covalent Modification. Proceedings of the National Academy of Sciences of the United States of America, 89 (15). pp. 6756-6760. ISSN 0027-8424. PMCID PMC49582. doi:10.1073/pnas.89.15.6756. https://resolver.caltech.edu/CaltechAUTHORS:BORpnas92

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Abstract

The Tar receptor is a transmembrane protein that regulates bacterial chemotaxis in response to changes in the level of aspartic acid in the medium. The extracellular portion of the protein can bind aspartate, and the cytoplasmic portion modulates CheA kinase activity. The receptor can either activate or inhibit the kinase. The cytoplasmic portion of the receptor can be modified by carboxymethylation of specific glutamic acid residues. To test the effects of differential methylation on receptor function, we prepared membranes from cells that have specifically modified forms of the receptor and tested the relative ability of each of these forms to activate or inhibit CheA kinase. Completely demethylated receptor was a potent inhibitor and poor activator of the kinase, while the fully modified receptor was an excellent activator but an inefficient inhibitor. Partially modified receptor could act both as an effective inhibitor and as an activator. Reversible modification provides a mechanism that allows the cell to accumulate a population of receptor molecules capable of generating a wide range of signaling intensities.


Item Type:Article
Related URLs:
URLURL TypeDescription
https://doi.org/10.1073/pnas.89.15.6756DOIArticle
http://www.ncbi.nlm.nih.gov/pmc/articles/pmc49582/PubMed CentralArticle
Additional Information:© 1992 by National Academy of Sciences Contributed by Melvin I. Simon, April 24, 1992 We would like to thank R. Stewart for plasmids and B. Bourret, M. Distefano, C. O'Day, A. Pakula, and T. Wilkie for helpful discussions and comments on the manuscript. This work was supported by National Institutes of Health Grants AI-19296 (M.I.S.) and GM-11223 (K.A.B.) and American Cancer Society Grant PF-3516 (L.A.A.). The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Funders:
Funding AgencyGrant Number
NIHAI-19296
NIHGM-11223
American Cancer SocietyPF-3516
Subject Keywords:chemotaxis, signal transduction, phosphorylation
Issue or Number:15
PubMed Central ID:PMC49582
DOI:10.1073/pnas.89.15.6756
Record Number:CaltechAUTHORS:BORpnas92
Persistent URL:https://resolver.caltech.edu/CaltechAUTHORS:BORpnas92
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:778
Collection:CaltechAUTHORS
Deposited By: Archive Administrator
Deposited On:30 Sep 2005
Last Modified:08 Nov 2021 19:05

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