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In both prokaryotes and eukaryotes methyl groups can be added to and removed from the carboxyl groups of proteins. Recent work has revealed that these reactions have a role in several behavioural phenomena. The nature of this role has been uncovered in one case--that of bacterial chemotaxis.
A high temperature conditional snake mutant, strain D1, of Agmenellum quadruplicatum was isolated which immediately stopped dividing following a shift to 41 degrees C following treatment with nitrosoguanidine. This mutant was stimulated to divide at 41 degrees C by the addition of inhibitors of RNA or protein synthesis: rifampicin, streptomycin, puromycin and chloramphenicol. Each of these inhibitors exhibited a discrete concentration optimum. The optimal concentration of chloramphenicol for cell division corresponded to the minimal concentrations necessary for the rapid inhibition of protein synthesis. The ability of chloramphenicol and other inhibitors to induce cell division in filaments decayed rapidly upon shifting to 30 degrees C. These results are interpreted as evidence for a protein acting as a negative regulator late in the cell cycle. At 41 degrees C, DNA was found distributed as a continuous zone throughout the length of the filaments. The addition of inhibitors of protein or RNA synthesis resulted in a rapid condensation of this nuclear material into multiple discrete nuclear regions suggesting that the negative control may be at the level of nuclear compartmentalization.
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The mechanism by which interference with the biosynthesis of bacterial cell wall causes death and lysis of bacteria appears more complex than originally thought. In an earlier model of the mode of action of beta-lactams, it was assumed that, in the presence of the antibiotics, bacteria synthesize a mechanically weak (poorly cross-linked) cell wall that ruptured under the osmotic-mechanical pressure of the normally growing cytoplasmic mass. However, recent findings suggest a much more complex picture. Lysis and, in at least some bacteria, loss of viability as well, seem to be catalyzed by autolytic enzymes (murein hydrolases), the destructive activity of which is triggered in the beta-lactam-treated bacterium via a poorly understood mechanism. Furthermore, different species of bacteria respond quite differently to treatment with the same beta-lactam: some bacteria are both killed and lysed, others only lose viability, whereas still other species respond mainly by a reversible inhibition of growth (beta-lactam-tolerant bacteria). In addition, structurally different beta-lactams may cause quite different biochemical, morphological, and antibacterial effects, even within the same bacterial species. It is conceivable, therefore, that there is more than one mechanism for loss of viability and/or lysis. Most of the bacteria examined so far contain a number (four to eight) of different penicillin-binding proteins. Genetic and physiological evidence obtained in E. coli indicate that these proteins play essential roles in a variety of physiological functions, such as maintenance of structural integrity, shape, and cell division. Pneumococci with a suppressed autolytic system are resistant to he lytic (and, partially at least, to the bactericidal) effect of beta-lactams. Interference with cell wall synthesis seems to trigger autolysin activity by upsetting the cellular control of autolytic enzyme. It is suggested that the irreversible antimicrobial effect of beta-lactams may have an indirect mechanism in other bacteria as well.
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Bacterial behavior is shown to be modulated through a simple on-off switching device which directs migration toward favorable conditions and away from unfavorable ones. The behavioral response is controlled by a rudimentary memory which allows the bacteria to sense gradients over time. The memory can be explained by a biochemical system involving a response regulator whose level relative to a threshold controls flagellar function. The level of the response regulator is itself controlled by factors such as enzyme levels and environmental stimuli. The molecular basis of the model appears to be relevant to more complex hormonal and neural signaling systems.
The two components of virginiamycin, virginiamycin M (VM) and virginiamycin S (VS), were used to explore the life cycle of symbiosis-dependent and -independent strains of Bdellovibrio bacteriovorus during multiplication in a two-membered system with either living or heat-inactivated Escherichia coli or in axenic cultures. Relatively high concentrations of these inhibitors separately were required to stop growth under all the conditions, but the minimum inhibitory concentration of the single components was reduced 1,000-fold by the association of VM and VS. No dissociation between mass growth and cell division was observed with VM; VS specifically halted cell division without affecting the kinetics of macromolecules formation and overall growth. This effect on cell division was only obtained when the antibiotic was added during the first half of the multiplication cycle and was reversible at any time.
Bacteria swim by rotating their flagella. They alter course by abruptly changing the direction of this rotation. The probability of the occurrence of this event is biased by chemoreception. The bias depends on the way in which the concentration of the attractant or repellent changes with time. Sugars are detected as they bind to specific proteins which also play a role in transport. The way in which the receptors are coupled to the flagella is not known. The coupling may involve changes in membrane potential.
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The effect of the disturbed correlation between the rates of synthesis of DNA and protein on the viability of bacterial cells was studied with different strain of E. coli K-12. The viability of the cells is determined by their resistance to sharp changes in the rates of synthesis of DNA and protein.