  We show how the competition between sensing and adaptation can result in a
performance peak in E.coli chemotaxis using extensive numerical simulations in
a detailed theoretical model. Receptor clustering amplifies the input signal
coming from ligand binding which enhances chemotactic efficiency. But large
clusters also induce large fluctuations in total activity since the number of
clusters go down. The activity and hence the run-tumble motility now gets
controlled by methylation levels which are part of adaptation module, rather
than ligand binding. This reduces chemotactic efficiency.
