UV radiation-induced enterobacterial responses, other processes that influence UV tolerance and likely environmental significance

• Published in: Science progress (1916) 2003-11, Vol.86 (4), p.313-332
• Main Author: ROWBURY, ROBIN J.
• Format: Article
• Language: English
• Subjects: Acid tolerance; Alkalies; Biological research; Biology, Experimental; Cell division; Deoxyribonucleic acid; DNA; DNA damage; DNA Damage - radiation effects; Enterobacter; Enterobacteriaceae; Enterobacteriaceae - genetics; Enterobacteriaceae - growth & development; Enterobacteriaceae - radiation effects; Environmental aspects; Food; Food and nutrition; Gene Expression Regulation - radiation effects; Genes, Bacterial - radiation effects; Genetic SOS response; Heat tolerance; Humans; Hydrogen peroxide; Immune tolerance; Irradiation; pH sensors; Radiation Tolerance - genetics; Sensors; Shellfish; Signal Transduction - radiation effects; Ultraviolet radiation; Ultraviolet Rays; Water treatment
• ISSN: 0036-8504; 2047-7163
• DOI: 10.3184/003685003783238644

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 tolerancespecific 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 f