Abstract
The ability of enterobacteria to become UV-tolerant is important because such tolerance may enable organisms to resist irradiation in the environment, in water treatment, in shell-fish, in stages of food processing, and at locations in the domestic, commercial and hospital environment The mechanism for regulation of tolerance induction and SOS response induction has been studied for many years, and is well understood, except for the early stages of induction. Such early stages, namely sensing of the stimulus (UV irradiation) and the way in which such sensing leads to signal production, have until now been poorly understood. The claim has been made that DNA is the sensor and that either damage to DNA or production of SS regions in DNA (following interaction of UV with DNA) triggers the signal that sets in train RecA activation and other stages of tolerance induction. This claimed induction mechanism is a “classical” one in the sense that it involves intracellular sensing (by DNA) of the stressing stimulus (UV), and production of an intracellular signalling molecule. It is not, however, firmly established as the mechanism for initiation of UV tolerance induction and SOS response induction. The results reviewed here give firm evidence for a different and unique mechanism for sensing of UV and production of the signal. These results establish without doubt that, for UV tolerance induction, the UV sensor is an extracellular protein, which is a UV tolerance-specific extracellular sensing component (ESC). This component is formed by unstressed cells and on interacting with the stimulus (UV) in the medium, is converted to the tolerance induction signalling molecule, which is a UV tolerance-specific extracellular induction component (EIC). It is this extracellular signal which interacts with the sensitive organisms and triggers tolerance induction. This pair of extracellular components (ECs) may offer the only means of switching-on such tolerance induction; certainly they offer the only known way for early warning to be given of impending UV challenge. Thus, the EIC can diffuse from a region of UV stress to a stress-free region and there warn organisms of impending stress and prepare them to resist it. As indicated here, UV irradiation not only induces UV tolerance, but also switches-on acid tolerance, alkali tolerance and thermotolerance responses. The fact that all three responses involve ESC/EIC pairs strongly supports the view that functioning of such EC pairs form the major, if not the only, means for UV tolerance induction. The UV tolerance-specific ESC can detect other stresses and becomes activated, leading to cross-tolerance responses. Of particular interest, this ESC acts as a biological thermometer, detecting increases in temperature, such increases leading to gradually increasing formation of the EIC and, accordingly, gradual increases in UV tolerance. This UV tolerance-specific ESC can also detect other stresses e.g acting as a pH sensor. In all cases, on activation, the EIC formed (from this specific ESC) only induces UV tolerance. It is proposed that the interaction of EICs with stress-sensitive organisms should be examined, and it is suggested that such EICs may, directly or indirectly, interact with and activate the same stress response regulators as are used to detect internal stressors and which, on activation, also trigger the switching-on of stress responses. For example, EICs either