Anaerobic Bacterial Response to Nitrosative Stress.

Abstract

This chapter provides an overview of current knowledge of how anaerobic bacteria protect themselves against nitrosative stress. Nitric oxide (NO) is the primary source of this stress. Aerobically its removal is an oxidative process, whereas reduction is required anaerobically. Mechanisms required to protect aerobic and anaerobic bacteria are therefore different. Several themes recur in the review. First, how gene expression is regulated often provides clues to the physiological function of the gene products. Second, the physiological significance of reports based upon experiments under extreme conditions that bacteria do not encounter in their natural environment requires reassessment. Third, responses to the primary source of stress need to be distinguished from secondary consequences of chemical damage due to failure of repair mechanisms to cope with extreme conditions. NO is generated by many mechanisms, some of which remain undefined. An example is the recent demonstration that the hybrid cluster protein combines with YtfE (or RIC protein, for repair of iron centres damaged by nitrosative stress) in a new pathway to repair key iron-sulphur proteins damaged by nitrosative stress. The functions of many genes expressed in response to nitrosative stress remain either controversial or are completely unknown. The concentration of NO that accumulates in the bacterial cytoplasm is essentially unknown, so dogmatic statements cannot be made that damage to transcription factors (Fur, FNR, SoxRS, MelR, OxyR) occurs naturally as part of a physiologically relevant signalling mechanism. Such doubts can be resolved by simple experiments to meet six proposed criteria.