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Receptor clustering as a cellular mechanism to control sensitivity

Author

Listed:
  • Dennis Bray

    (University of Cambridge)

  • Matthew D. Levin

    (University of Cambridge)

  • Carl J. Morton-Firth

    (University of Cambridge)

Abstract

Chemotactic bacteria such as Escherichia coli can detect and respond to extremely low concentrations of attractants, concentrations of less than 5 nM in the case of aspartate1. They also sense gradients of attractants extending over five orders of magnitude in concentration (up to 1 mM aspartate)2,3. Here we consider the possibility that this combination of sensitivity and range of response depends on the clustering of chemotactic receptors on the surface of the bacterium4. We examine what will happen if ligand binding changes the activity of a receptor, propagating this change in activity to neighbouring receptors in a cluster5,6. Calculations based on these assumptions show that sensitivity to extracellular ligands increases with the extent of spread of activity through an array of receptors, but that the range of concentrations over which the array works is severely diminished. However, a combination of low threshold of response and wide dynamic range can be attained if the cell has both clusters and single receptors on its surface, particularly if the extent of activity spread can adapt to external conditions. A mechanism of this kind can account quantitatively for the sensitivity and response range of E. coli to aspartate.

Suggested Citation

  • Dennis Bray & Matthew D. Levin & Carl J. Morton-Firth, 1998. "Receptor clustering as a cellular mechanism to control sensitivity," Nature, Nature, vol. 393(6680), pages 85-88, May.
    • Handle: RePEc:nat:nature:v:393:y:1998:i:6680:d:10.1038_30018
    DOI: 10.1038/30018
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    Citations

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    Cited by:

    1. Diana Clausznitzer & Olga Oleksiuk & Linda Løvdok & Victor Sourjik & Robert G Endres, 2010. "Chemotactic Response and Adaptation Dynamics in Escherichia coli," PLOS Computational Biology, Public Library of Science, vol. 6(5), pages 1-11, May.
    2. Tristan Ursell & Kerwyn Casey Huang & Eric Peterson & Rob Phillips, 2007. "Cooperative Gating and Spatial Organization of Membrane Proteins through Elastic Interactions," PLOS Computational Biology, Public Library of Science, vol. 3(5), pages 1-10, May.
    3. Robert G Endres & Joseph J Falke & Ned S Wingreen, 2007. "Chemotaxis Receptor Complexes: From Signaling to Assembly," PLOS Computational Biology, Public Library of Science, vol. 3(7), pages 1-9, July.
    4. Kenneth L Ho & Heather A Harrington, 2010. "Bistability in Apoptosis by Receptor Clustering," PLOS Computational Biology, Public Library of Science, vol. 6(10), pages 1-9, October.
    5. Stephan Eismann & Robert G Endres, 2015. "Protein Connectivity in Chemotaxis Receptor Complexes," PLOS Computational Biology, Public Library of Science, vol. 11(12), pages 1-21, December.
    6. Christopher T Lee & Justin G Laughlin & Nils Angliviel de La Beaumelle & Rommie E Amaro & J Andrew McCammon & Ravi Ramamoorthi & Michael Holst & Padmini Rangamani, 2020. "3D mesh processing using GAMer 2 to enable reaction-diffusion simulations in realistic cellular geometries," PLOS Computational Biology, Public Library of Science, vol. 16(4), pages 1-35, April.
    7. Derek J Cashman & Davi R Ortega & Igor B Zhulin & Jerome Baudry, 2013. "Homology Modeling of the CheW Coupling Protein of the Chemotaxis Signaling Complex," PLOS ONE, Public Library of Science, vol. 8(8), pages 1-9, August.

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