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Receptor clustering as a cellular mechanism to control sensitivity

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.

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Figure 1: Activity spread in a cluster of receptors.
Figure 2: Changes in the response to threshold and range of ligand concentration with the extent of activity spread.

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Acknowledgements

We thank M. Keeling for help with mathematics, S. Khan for permission to cite unpublished data, and R. Bourret, E. Siggia and T. Lamb for criticisms of the manuscript.

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Correspondence to Dennis Bray.

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Bray, D., Levin, M. & Morton-Firth, C. Receptor clustering as a cellular mechanism to control sensitivity. Nature 393, 85–88 (1998). https://doi.org/10.1038/30018

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