Plant mechanism of an adaptive stress response homologous to bacterial stringent response

All living organisms possess adaptive responses to environmental stresses that are essential to ensuring cell survival. One of them is the stringent response, initially discovered forty years ago in the gram-negative model organism E. coli. Recently plant homologues to the bacterial relA/spoT genes were identified (RSH genes--RelA/SpoT Homologues). Also the products of rsh proteins activity--(p)ppGpp were identified in the chloroplasts of plant cells. Levels of ppGpp increased markedly when plants were subjected to some biotic and abiotic stresses. Elevation of ppGpp levels was elicited also by treatment with plant hormones. What is more--in vitro, chloroplast RNA polymerase activity was inhibited in the presence of ppGpp. It is supposed that plant stringent response is a conserve stress-response pathway possibly operating via regulation of chloroplast gene expression and, thus, the regulation of plastid metabolism.     

Antitoxin MqsA helps mediate the bacterial general stress response

Although it is well recognized that bacteria respond to environmental stress through global networks, the mechanism by which stress is relayed to the interior of the cell is poorly understood. Here we show that enigmatic toxin-antitoxin systems are vital in mediating the environmental stress response. Specifically, the antitoxin MqsA represses rpoS, which encodes the master regulator of stress. Repression of rpoS by MqsA reduces the concentration of the internal messenger 3,5-cyclic diguanylic acid, leading to increased motility and decreased biofilm formation. Furthermore, the repression of rpoS by MqsA decreases oxidative stress resistance via catalase activity. Upon oxidative stress, MqsA is rapidly degraded by Lon protease, resulting in induction of rpoS. Hence, we show that external stress alters gene regulation controlled by toxin-antitoxin systems, such that the degradation of antitoxins during stress leads to a switch from the planktonic state (high motility) to the biofilm state (low motility).     

Evolution: bacterial mutation in stationary phase

A recent study indicates that the genomic mutation rate of the gut bacterium Escherichia coli is substantially higher in nongrowing than growing cultures. These findings are important in the light of the ongoing controversy over the generality and robustness of stationary phase mutagenesis and its evolutionary implications.     

Aspects of cellular biology of the bacterial stationary phase: programmed cell death and regulation by guanosine tetraphosphate

The paper discusses (1) programmed cell death, the phenomenon typical of the stationary phase of bacteria occurring under unfavorable conditions, (2) its pleiotropic regulation by guanosine tetraphosphate, and (3) the conception of "addiction module," a specific genetic system responsible for the cell choice between survival and death under unfavorable conditions. The shortcomings of the proposed interpretation of the problem at hand are considered and the necessity of their further investigation is substantiated.     

Pyoverdin cheats fail to invade bacterial populations in stationary phase

Microbes engage in cooperative behaviours by producing and secreting public goods, the benefits of which are shared among cells, and are therefore susceptible to exploitation by nonproducing cheats. In nature, bacteria are not typically colonizing sterile, rich environments in contrast to laboratory experiments, which involve inoculating sterile culture with few bacterial cells that then race to fill the available niche. Here, we study the potential implications of this difference, using the production of pyoverdin, an iron‐scavenging siderophore that acts as a public good in the bacteria Pseudomonas aeruginosa. We show that (1) nonproducers are able to invade cultures of producers when added at the start of growth or during early exponential growth phase, but not during late exponential or stationary phase; (2) the producer strain does not produce pyoverdin in the late exponential and stationary phases and so is not paying the cost of cooperating during those phases. These results suggest that whether a nonproducing mutant can invade will depend upon when the mutation arises, as well as the population structure, and raise a potential difficulty with the use of antimicrobial treatment strategies that propose to exploit the invasive abilities of cheats.     

细菌的光响应及其机制研究进展

光作为一种环境信号,对细菌的生长和代谢有广泛的调节作用。对于光合细菌来讲,一方面,感光蛋白可以协助光合细菌游向最适的光环境,以利于其细胞内的光系统进行光合作用;另一方面,一些光合细菌可以感受并捕获光能为代谢提供能量。目前发现有些非光合细菌也有光响应,感光蛋白在细菌基因组内是普遍存在的,而且与细菌的一些生理功能有关。本文以非光合细菌为主介绍了目前在细菌中发现的趋光现象及其响应机制。     

ColD-derived cloning vectors that autoamplify in the stationary phase of bacterial growth

The construction of cloning vectors based on the replicon of plasmid ColD-CA23 is reported. These vectors, like ColD itself, autoamplify when cultures of host bacteria enter the stationary phase of growth, thereby resulting in a substantial increase in the expression of cloned genes as a consequence of the increase in gene dosage. The principal advantage of these vectors is that, unlike the situation pertaining to other expression vectors, the increase in expression of genes cloned in ColD vectors does not require any experimental intervention (i.e., occurs naturally), and takes place at high cell densities. The vectors show high stability in Escherichia coli strains and are compatible with ColE1-type cloning vectors.     

Introduction to proteomics: tools for the new biology

Towards revolutionary biomarkers, a considerable amount of research funds and time have been dedicated to proteomics. Although the discovery of novel biomarkers at the dawn of proteomics was a promising development, only a few identified biomarkers seemed to be beneficial for cancer patients. We may need to approach this issue differently, instead of only extending the conventional approaches that have been used historically. The study of biomarkers is essentially a study of diseases and the biochemistry relating to peptide, protein and post-translational modifications is only a tool. A problem-oriented approach should be needed in biomarker development. Clinician participation in the study of biomarkers will lead to realistic, practical and interesting biomarker candidates, which justify the time and expense involved in validation studies. Although discussion in this article is focused on cancer biomarkers, it can generally be applied to biomarker studies for other diseases.