Other issues such as breaking of cell axial symmetry by formation of surface TC-MCH 7c contact or a reduction in the amount of cell surface exposed to external medium and fluid flows could also be taken into consideration when formulating new working hypotheses for elucidating surface sensing mechanisms. Our results, which associate respiration reduction with surface sensing, also raise the question of the role of that event in surface contact signaling. Recently, a contact-dependent growth inhibition process involving metabolic down-modulation upon cell-cell contact was discovered in E. coli. This phenomenon �� mediated by surface-specific protein recognition in an asymmetric inhibitor/target contact involving the immunity protein and toxin translocation across target cell envelopes �� is assuredly different from the one observed here. However, it provides an example of a contact-driven bacterial response pathway in which metabolic parameters are reduced in the absence of TCS 1105 nutrient deprivation. Moreover, Aoki and co-workers suggested that a respiration decrease could be a general response to formation of physical contact at the cell surface; they proposed that respiration reduction could enable survival under conditions of oxidative stress. Thus far, to the best of our knowledge, no experimental evidence supporting a molecular mechanism linking respiration reduction and contact formation has been published. Conversely, other authors detected metabolism stimulation events upon surface adhesion. However, their experiments were performed under 12 h starvation conditions, thus significantly differing from our own experimental conditions. Here we provide new tools for investigating in more detail this metabolic shift induced by surface contact at the single-cell level. Our approach enables discriminating between sensing mediated by soluble secreted factors and direct physical cell surface contact by monitoring planktonic and attached cells exposed in parallel to the same medium. This is a key issue in the better understanding of the mechanisms driving adherent cell transition towards an altered physiological state. Our results indicate that the reduction in the cell respiration level participates in early signaling triggered upon cell aggregation or settlement on an artificial substrate. These results raise many questions for further investigation. What is the impact of this reduction on overall cell functioning, and, for instance, on the cell division rate? Is this a way for cells growing in the form of attached communities to achieve greater tolerance to oxidative stress or to various antimicrobials? What are the molecular bases for this contact-dependent behavior?