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Bacterial Stress Response

The Experts below are selected from a list of 282 Experts worldwide ranked by ideXlab platform

Meta J Kuehn – 1st expert on this subject based on the ideXlab platform

  • biological functions and biogenesis of secreted Bacterial outer membrane vesicles
    Annual Review of Microbiology, 2010
    Co-Authors: Adam Kulp, Meta J Kuehn


    Gram-negative bacteria produce outer membrane vesicles (OMVs) that contain biologically active proteins and perform diverse biological processes. Unlike other secretion mechanisms, OMVs enable bacteria to secrete insoluble molecules in addition to and in complex with soluble material. OMVs allow enzymes to reach distant targets in a concentrated, protected, and targeted form. OMVs also play roles in Bacterial survival: Their production is a Bacterial Stress Response and important for nutrient acquisition, biofilm development, and pathogenesis. Key characteristics of OMV biogenesis include outward bulging of areas lacking membrane-peptidoglycan bonds, the capacity to upregulate vesicle production without also losing outer membrane integrity, enrichment or exclusion of certain proteins and lipids, and membrane fission without direct energy from ATP/GTP hydrolysis. Comparisons of similar budding mechanisms from diverse biological domains have provided new insight into evaluating mechanisms for outer membrane vesiculation.

  • release of outer membrane vesicles by gram negative bacteria is a novel envelope Stress Response
    Molecular Microbiology, 2007
    Co-Authors: Amanda J Mcbroom, Meta J Kuehn


    Conditions that impair protein folding in the Gram-negative Bacterial envelope cause Stress. The destabilizing effects of Stress in this compartment are recognized and countered by a number of signal transduction mechanisms. Data presented here reveal another facet of the complex Bacterial Stress Response, release of outer membrane vesicles. Native vesicles are composed of outer membrane and periplasmic material, and they are released from the Bacterial surface without loss of membrane integrity. Here we demonstrate that the quantity of vesicle release correlates directly with the level of protein accumulation in the cell envelope. Accumulation of material occurs under Stress, and is exacerbated upon impairment of the normal housekeeping and Stress-responsive mechanisms of the cell. Mutations that cause increased vesiculation enhance Bacterial survival upon challenge with Stressing agents or accumulation of toxic misfolded proteins. Preferential packaging of a misfolded protein mimic into vesicles for removal indicates that the vesiculation process can act to selectively eliminate unwanted material. Our results demonstrate that production of Bacterial outer membrane vesicles is a fully independent, general envelope Stress Response. In addition to identifying a novel mechanism for alleviating Stress, this work provides physiological relevance for vesicle production as a protective mechanism.

Wilson A Coulter – 2nd expert on this subject based on the ideXlab platform

  • Bacterial Stress Response to environmental radiation relating to the fukushima radiation discharge event japan will environmental bacteria alter their antibiotic susceptibility profile
    Ecotoxicology and Environmental Safety, 2012
    Co-Authors: Shigeyuki Nakanishi, John E Moore, M Matsuda, Colin E Goldsmith, Wilson A Coulter


    Abstract Antibiotic resistance in clinical pathogens in humans may be traced back to resistance mechanisms in environmental bacteria and any factors, which are likely to alter (upregulate) resistance in environmental organisms, is of potential and eventual consequence to human pathogens. Furthermore, sublethal doses of gamma radiation to environmental organisms may cause sublethal Stress and a selective pressure, which may lead to mutational events that alter the bacterium’s susceptibility profile. A gamma ( γ ) radiation simulation experiment was performed to emulate the exposure of four environmental bacteria, including Listeria innocua , Bacillus subtilis , E. coli and Pseudomonas aeruginosa , to levels of radiation in and around Fukushima, Japan, equating to 1, 10 and 100 years equivalence exposure. Alteration to susceptibility to 14 antibiotics was measured as the primary endpoint. There was no significant alteration in the susceptibility of the Gram-positive organisms, whereas both Gram-negative organisms became slightly more susceptible to the antibiotics tested over time. These data indicate that such radiation exposure will not increase the antibiotic resistance profile of these organisms and hence not add to the global public health burden of increased antibiotic resistance in human Bacterial pathogens.

Etienne Maisonneuve – 3rd expert on this subject based on the ideXlab platform

  • YtfK activates the stringent Response by triggering the alarmone synthetase SpoT in Escherichia coli
    Nature Communications, 2019
    Co-Authors: Elsa Germain, Paul Guiraud, Deborah Byrne, Badreddine Douzi, Meriem Djendli, Etienne Maisonneuve


    The enzyme SpoT is important for accumulation of the alarmone (p)ppGpp, which triggers the stringent Response in E. coli . Here, Germain et al. show that the protein YtfK promotes SpoT-dependent accumulation of (p)ppGpp and is required for activation of the stringent Response during phosphate and fatty acid starvation. The stringent Response is a general Bacterial Stress Response that allows bacteria to adapt and survive adverse conditions. This reprogramming of cell physiology is caused by the accumulation of the alarmone (p)ppGpp which, in Escherichia coli , depends on the (p)ppGpp synthetase RelA and the bifunctional (p)ppGpp synthetase/hydrolase SpoT. Although conditions that control SpoT-dependent (p)ppGpp accumulation have been described, the molecular mechanisms regulating the switching from (p)ppGpp degradation to synthesis remain poorly understood. Here, we show that the protein YtfK promotes SpoT-dependent accumulation of (p)ppGpp in E. coli and is required for activation of the stringent Response during phosphate and fatty acid starvation. Our results indicate that YtfK can interact with SpoT. We propose that YtfK activates the stringent Response by tilting the catalytic balance of SpoT toward (p)ppGpp synthesis.