Science Progress

The role of the bacterial ribosome in the cellular response to environmental stress has been widely considered over last decade. Certain ribosome-associated proteins have been shown to induce conformational changes that lead to the formation of inactive forms of ribosomes that are presumed to be more stable during stationary phase. This was found to aid the survival of bacteria in this phase. Such proteins include ribosome modulation factor (RMF), YfiA and YhbH. Examining the influence of RMF on the survival of E. coli under heat, acid and osmotic stress showed that it was important for bacterial viability under these environmental pressures. However, the mechanism by which this protein exerts its effect has not been fully elucidated. The present work reviews the involvement of ribosomes in determining cell behaviour during stress. It focuses on the action of the ribosome-associated proteins and their role in inactivating ribosomes for preserving their integrity and aiding cell survival under stress.

Bacterial cells have adapted in a variety of ways to resist oxidative stresses and damage in their everyday lives in a predominantly aerobic world. The nearly universal occurrence of resistance mechanisms against oxidative stresses, particularly those due to reactive oxygen species (ROS), suggests that most, if not all, bacteria have to deal with oxidative assaults. A primary source of oxidative stress is aerobic metabolism, which leads to production of ROS such as hydrogen peroxide, superoxide radical, perhydroxyl radical, hydroxyl radical and a variety of other toxic metabolites, including organic peroxides and other organics or inorganics able to transfer electrons to sites of oxidative damage. Anaerobes as well as aerobic and facultative organisms are subject to oxidative stresses, often as a result of their own metabolism of O₂ or that of associated facultative organisms. If anaerobes would just ignore oxygen instead of metabolizing it, they would not have to deal with toxic metabolites of their own making. Another major source of oxidative stress comes from the use of oxidative agents in the disinfection-sterilization industry. Notable examples are hypochlorite for water purification and hydrogen peroxide used for industrial sterilization. Antimicrobials such as isoniazide and mitomycin C also act oxidatively to cause damage. In this article, aseptic packaging and processing involving use of hydrogen peroxide for sterilization of packaging materials is reviewed as an example of oxidative stress imposed on bacterial spores and vegetative cells from outside the organisms or the microbial community. The other example considered is related to oral microbiology and infectious disease in which oxidative stress may arise from the metabolism of the oral microbiota or may come from outside through use of oral care products.

There are several unusual features about phage when you first encounter them as a biologist. They are small, but conform to one of a few morphological types. Next their genomes can be composed of DNA or RNA and be single or double stranded. Finally they are numerically more abundant than prokaryotes and a significant proportion of them form an association in their microbial host populations termed lysogeny. The latter findings indicate that they are numerically significant in microbial populations. Since bacterial and phage abundance or lack of it is related in environments, this implies that the phage populations ‘titrate’ their hosts, and more probably the host's physiological status. Microbial populations wax and wane with nutritional inputs and there is a dynamic relationship between phage population sizes and host numbers and physiology. Overlay this with the different phage life cycle strategies, exemplified at the extremes by phage lambda (temperate) and phage T4 (virulent), then it becomes apparent that phage are a component in nutrient cycling in ecology. But their contribution does not stop there. Many are capable of transduction, moving DNA from one cell into another. So they can also aid the evolutionary progress of microbial populations by allowing them to share genes, just as gene exchange via plasmids and transformation does. Our perception of bacteria has been derived from pure culture studies and we are just being able to appreciate how subtle their ecological interactions are. This is no less true of the studies on bacteriophage, which are almost all based on laboratory experimentation, where the hosts are physiologically stressed by growing in ‘high nutritional and optimum conditions’. The natural environment is naturally discontinuous and life evolved in this. Thus our perceptions of bacteriophage and their life cycle patterns derived from laboratory experimentation may be a little off the mark when we come to understand how they and their hosts interact in the niches available to them. It is worth just considering this as you read the article, as I suspect phage behaviours are more intimately involved in, and moderated by the physiological stresses in the life cycle of bacteria than we currently believe.

Several striking findings, related to biological effects of external acidity, are reviewed here. The first of these relates to the role of PhoE in the penetration of H⁺ and protonated metabolites into the cell. PhoE is an anion pore and would not be expected to take up protons. The work reviewed here, however, shows that the loss or repression of PhoE leads to poor H⁺ passage through the outer membrane (OM), whilst derepression of PhoE leads to facilitated passage. It is now believed that H⁺ crosses through the PhoE pore in association possibly with oligopeptides, and that other protonated molecules, such as the acid tolerance EIC, use the same means to cross the OM. Additionally, several processes that form early warning systems against acidity are reviewed here. First, the properties of the acid tolerance EIC alarmones allow them to diffuse to regions not yet facing acid stress, and there give early warning and induce sensitive organisms to tolerance. Second, some agents, such as glucose, induce acid tolerance in organisms, long before these organisms are exposed to catabolically-produced acidity, preparing them, in advance, to resist this impending acid challenge. Third, the occurrence of multiple forms of ESCs (i.e. of varisensors) ensures that where organisms have been grown under conditions that sensitise them to acid stress, the ESCs formed are modified so as to be activated at much higher pH values, ensuring that lethality by acid is reduced or abolished. Fourthly, normally only EICs induce tolerance. Strikingly, however, pH 8.5 or 9.0-grown cells are induced to tolerance by ESC formed at pH 6.5. This is believed to provide another early warning system, protecting alkali-grown cells against sudden acidification of media. Two other finding reviewed here should be emphasised. First, the hydrophobic antibiotic novobiocin is ineffective against enterobacteria, due to its failure to penetrate the OM barrier. This only applies to cultures in pH 7.0 media, however, cells growing at pH 5.0 being exquisitely sensitive to novobiocin, due to a conformational change to the antibiotic at acidic pH, which allows ready penetration through the OM. Second, acidic pHs affect the synthesis and effects of another antibiotic, namely colicin V. Thus pH 5.0 prevents both synthesis of this agent and its effects on sensitive cells. Exposure to external acidity leads to numerous other effects, including those that influence growth, cell division, plasmid transfer and chemotaxis; these have also been reviewed here.