Robert Hooke, 1635-1703.

Robert Hooke was a polymath whose expertise during the 17th century spanned many different scientific areas. As a schoolboy on the Isle of Wight he was obsessed with the possibility of human flight and later became equally absorbed in cosmology and planetary motion. His skills as an artist were put to good use both as an architect following the Great Fire of London and before that in Micrographia.

Extracellular sensors and extracellular alarmones, which permit cross-talk between organisms, determine the levels of alkali tolerance and trigger alkaliinduced acid sensitivity in Escherichia coli.

For several stress responses in Escherichia coli, switching on involves conversion by the stress of an extracellular stress sensor (an extracellular sensing component, ESC) to an extracellular induction component (EIC), the latter functioning as an alarmone and inducing the response. The aim of this study was to establish whether alkali tolerance induction at pH 9.0, alkali sensitisation induced at pH 5.

Intracellular and extracellular components as bacterial thermometers, and early warning against thermal stress.

Responses induced by cold or heat are triggered following detection of temperature changes by specific sensing molecules, complexes or structures. Low temperature responses are often induced following sensing of cold-induced falls in membrane fluidity, such changes turning-on or -off enzymic activities in membrane proteins, although ribosomes and DNA may also function in cold perception. Many thermal sensors are components of structures damaged by the heat, with sensing involving changes to ribosomes, DNA, intracellular proteins and, less commonly, membrane fluidity.

Enterobacterial responses to external protons, including responses that involve early warning against stress and the functioning of extracellular pheromones, alarmones and varisensors.

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.

Characterisation of viridans group streptococci with different levels of Tet(M)-mediated tetracycline resistance.

Streptococcus oralis 264-3, Streptococcus mitis 254-1 and S. mitis 264-1, isolated from the oral cavities of two children were each found to carry the tet(M) gene but exhibited different degrees of reduced susceptibility to tetracycline (tetracycline MICs of 2, 8 and 64 mg/L, respectively). The aim of this study was to determine the molecular basis for the different levels of tetracycline resistance (Tc(R)) observed.

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

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.

Mercuric resistance genes in gram-positive oral bacteria.

Mercury-resistant bacteria isolated from the oral cavities of children carried one of two types of merA gene that appear to have evolved from a common ancestor. Streptococcus oralis, Streptococcus mitis and a few other species had merA genes that were very similar to merA of Bacillus cereus strain RC607. Unlike the B.

How killed enterobacterial cultures can activate living organisms to resist lethal agents or conditions.

A major aim in many areas of microbiology is to ensure sterility, and even where this is impossible, to reduce the number of viable organisms occurring in particular environments to an absolute minimum. This applies in the aquatic environment, where e.g.

Extracellular proteins as enterobacterial thermometers.

Biological thermometers are cellular components or structures which sense increasing temperatures, interaction of the thermometer and the thermal stress bringing about the switching-on of inducible responses, with gradually enhanced levels of response induction following gradually increasing temperatures. In enterobacteria, for studies of such thermometers, generally induction of heat shock protein (HSP) synthesis has been examined, with experimental studies aiming to establish (often indirectly) how the temperature changes which initiate HSP synthesis are sensed; numerous other processes and responses show graded induction as temperature is increased, and how the temperature changes which induce these are sensed is also of interest. Several classes of intracellular component and structure have been proposed as enterobacterial thermometers, with the ribosome and the DnaK chaperone being the most favoured, although for many of the proposed intracellular thermometers, most of the evidence for their functioning in this way is indirect.

Morphological changes to Escherichia coli O157:H7, commensal E. coli and Salmonella spp in response to marginal growth conditions, with special reference to mildly stressing temperatures.

Certain rod-shaped bacteria have been reported to form elongated filamentous cells when exposed to marginal growth conditions, including refrigeration temperatures. To expand upon these observations, the filamentation of commensal Escherichia coli, E. coli O157:H7 and Salmonella spp was investigated, following exposure to certain, mildly stressing, levels of temperature, pH or water activity (aw), with levels of cellular protein being monitored during cell elongation, in some experiments.

Effect of restoration of children's teeth with mercury amalgam on the prevalence of mercury- and antibiotic-resistant oral bacteria.

The purpose of this study was to determine whether placement of mercury amalgam restorations in children's teeth induces an increase in oral bacteria resistant to mercury, penicillin, ampicillin, erythromycin, or tetracycline. Dental plaque and saliva samples from 16 children without mercury amalgam restorations were screened for bacteria resistant to mercury or to one of the antibiotics prior to, and 1 month after, placement of the amalgam restoration. Following amalgam placement, there was no significant increase in the number of children harboring bacteria resistant to mercury, penicillin, ampicillin, erythromycin, or tetracycline; neither was there an increase in the proportions of such organisms.

Effect of medium composition on the susceptibility of oral streptococci to mercuric chloride.

Although there is considerable interest in identifying mercury-resistant bacteria, no standardized assay exists for this purpose. In this study, the effect of the composition of the medium on the susceptibility of oral streptococci to HgCl(2) was investigated. The minimum inhibitory concentration (MIC) of HgCl(2) for 52 streptococcal strains and the reproducibility of MIC values for Hg-sensitive and Hg-resistant strains was determined with 11 different media.

Prevalence and antibiotic resistance profile of mercury-resistant oral bacteria from children with and without mercury amalgam fillings.

Genes encoding resistance to mercury and to antibiotics are often carried on the same mobile genetic element and so it is possible that mercury-containing dental materials may select for bacteria resistant to mercury and to antibiotics. The main aim of this study was to determine whether the prevalence of Hg-resistant oral bacteria was greater in children with mercury amalgam fillings than in those without. A secondary aim was to determine whether the Hg-resistant isolates were also antibiotic resistant.

Extracellular sensing and signalling pheromones switch-on thermotolerance and other stress responses in Escherichia coli.

The findings reviewed here overturn a major tenet of bacterial physiology, namely that stimuli which switch-on inducible responses are always detected by intracellular sensors, with all other components and stages in induction also being intracellular. Such an induction mechanism even applies to quorum-sensed responses, and some others which involve functioning of extracellular components, and had previously been believed to occur in all cases. In contrast, for the stress responses reviewed here, triggering is by a quite distinct process, pairs of extracellular components being involved, with the stress sensing component (the extracellular sensing component, ESC) and the signalling component, which derives from it and induces the stress (the extracellular induction component, EIC), being extracellular and the stimulus detection occurring in the growth medium.

Extracellular sensing components and extracellular induction component alarmones give early warning against stress in Escherichia coli.

The work reported here follows from the proposal that, for efficient induction of numerous extracellular stress responses, cultures contain extracellular stress-sensing molecules, termed extracellular sensing components (ESCs). These are directly converted to extracellular induction components (EICs) by stresses, thus providing an early warning system against stress, with very rapid responses occurring on exposure to increasing levels of stress. Although some stress responses appear to involve activation of intracellular sensors, the proposed ESCs and EICs function for many stress tolerance and sensitization responses and for several cross-tolerance and cross-sensitization responses.

An extracellular sensor and an extracellular induction component are required for alkali induction of alkyl hydroperoxide tolerance in Escherichia coli.

Escherichia coli K12 transferred from pH 7.0 to pH 9.0 gains alkylhydroperoxide (AHP) tolerance.