The energy level of a cell is determined by the state of three interconvertible components: ATP, the proton motive force, and the redox level of the electron transport chain. Oxygen taxis, oxidizable substrate taxis and phototaxis are all behaviors governed by sensing of the energy level. This research will identify the energy-level sensor of E. coli and establish the principal mechanism of sensing. An arcB mutant fails to show O2- taxis and oxidizable substrate (proline) taxis. A cloned arcB locus will be used to identify the sensor by expressing and localizing the arcB product. By comparing cell responses to CN and uncoupler that similarly decrease the pmf, but have different effects on the redox state, it will be found whether a redox chain component or pmf per se are immediately responsible for energy level sensing. Understanding of information transduction will be achieved by isolating pseudorevertants to arcB that will map in a che gene(s). This study bridges two fields of knowledge: metabolic regulation and behavior, since arcB controls both taxis and O2-dependent transcription. It is highly possible that arcB (or a homologous compound) is additionally responsible for other instances of so-called "pmf-dependent" regulation in various bacteria, as well as in mitochondria and chloroplasts. It is of fundamental significance to learn how the bacterial cell senses its own energy level and uses this information to control behavior. A new type of sensor which is substantially different from known sensors will be explored in this study. The principal mechanism of energy level sensing will be elucidated. Since it is possible that mitochondria and chloroplasts "inherited" the energy level sensor from bacteria, this research may provide a model system for studying behavior of higher organisms.
