Journal articles: 'Stress response of bacteria'

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Bonilla, Carla Y. "Generally Stressed Out Bacteria: Environmental Stress Response Mechanisms in Gram-Positive Bacteria." Integrative and Comparative Biology 60, no. 1 (February 11, 2020): 126–33. http://dx.doi.org/10.1093/icb/icaa002.

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Abstract The ability to monitor the environment for toxic chemical and physical disturbances is essential for bacteria that live in dynamic environments. The fundamental sensing mechanisms and physiological responses that allow bacteria to thrive are conserved even if the molecular components of these pathways are not. The bacterial general stress response (GSR) represents a conceptual model for how one pathway integrates a wide range of environmental signals, and how a generalized system with broad molecular responses is coordinated to promote survival likely through complementary pathways. Environmental stress signals such as heat, osmotic stress, and pH changes are received by sensor proteins that through a signaling cascade activate the sigma factor, SigB, to regulate over 200 genes. Additionally, the GSR plays an important role in stress priming that increases bacterial fitness to unrelated subsequent stressors such as oxidative compounds. While the GSR response is implicated during oxidative stress, the reason for its activation remains unknown and suggests crosstalk between environmental and oxidative stress sensors and responses to coordinate antioxidant functions. Systems levels studies of cellular responses such as transcriptomes, proteomes, and metabolomes of stressed bacteria and single-cell analysis could shed light into the regulated functions that protect, remediate, and minimize damage during dynamic environments. This perspective will focus on fundamental stress sensing mechanisms and responses in Gram-positive bacterial species to illustrate their commonalities at the molecular and physiological levels; summarize exciting directions; and highlight how system-level approaches can help us understand bacterial physiology.

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Chowdhury, Rukhsana, Gautam K. Sahu, and Jyotirmoy Das. "Stress response in pathogenic bacteria." Journal of Biosciences 21, no. 2 (April 1996): 149–60. http://dx.doi.org/10.1007/bf02703105.

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Poisot, Timothée, Thomas Bell, Esteban Martinez, Claire Gougat-Barbera, and Michael E. Hochberg. "Terminal investment induced by a bacteriophage in a rhizosphere bacterium." F1000Research 1 (October 2, 2012): 21. http://dx.doi.org/10.12688/f1000research.1-21.v1.

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Despite knowledge about microbial responses to abiotic stress, few studies have investigated stress responses to antagonistic species, such as competitors, predators and pathogens. While it is often assumed that interacting populations of bacteria and phage will coevolve resistance and exploitation strategies, an alternative is that individual bacteria tolerate or evade phage predation through inducible responses to phage presence. Using the microbial modelPseudomonas fluorescensSBW25 and its lytic DNA phage SBW25Φ2, we demonstrate the existence of an inducible response in the form of a transient increase in population growth rate, and found that the response was induced by phage binding. This response was accompanied by a decrease in bacterial cell size, which we propose to be an associated cost. We discuss these results in the context of bacterial ecology and phage-bacteria co-evolution.

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Poisot, Timothée, Thomas Bell, Esteban Martinez, Claire Gougat-Barbera, and Michael E. Hochberg. "Terminal investment induced by a bacteriophage in a rhizosphere bacterium." F1000Research 1 (May 20, 2013): 21. http://dx.doi.org/10.12688/f1000research.1-21.v2.

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Despite knowledge about microbial responses to abiotic stress, few studies have investigated stress responses to antagonistic species, such as competitors, predators and pathogens. While it is often assumed that interacting populations of bacteria and phage will coevolve resistance and exploitation strategies, an alternative is that individual bacteria tolerate or evade phage predation through inducible responses to phage presence. Using the microbial modelPseudomonas fluorescensSBW25 and its lytic DNA phage SBW25Φ2, we demonstrate the existence of an inducible response in the form of a transient increase in population growth rate, and found that the response was induced by phage binding. This response was accompanied by a decrease in bacterial cell size, which we propose to be an associated cost. We discuss these results in the context of bacterial ecology and phage-bacteria co-evolution.

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YAMAMOTO, Tomoko. "Stress Response of Pathogenic Bacteria. Are Stress Proteins Virulence Factors?" Nippon Saikingaku Zasshi 51, no. 4 (1996): 1025–36. http://dx.doi.org/10.3412/jsb.51.1025.

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Si, Meiru, Chao Zhao, Brianne Burkinshaw, Bing Zhang, Dawei Wei, Yao Wang, Tao G. Dong, and Xihui Shen. "Manganese scavenging and oxidative stress response mediated by type VI secretion system in Burkholderia thailandensis." Proceedings of the National Academy of Sciences 114, no. 11 (February 27, 2017): E2233—E2242. http://dx.doi.org/10.1073/pnas.1614902114.

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Type VI secretion system (T6SS) is a versatile protein export machinery widely distributed in Gram-negative bacteria. Known to translocate protein substrates to eukaryotic and prokaryotic target cells to cause cellular damage, the T6SS has been primarily recognized as a contact-dependent bacterial weapon for microbe–host and microbial interspecies competition. Here we report contact-independent functions of the T6SS for metal acquisition, bacteria competition, and resistance to oxidative stress. We demonstrate that the T6SS-4 in Burkholderia thailandensis is critical for survival under oxidative stress and is regulated by OxyR, a conserved oxidative stress regulator. The T6SS-4 is important for intracellular accumulation of manganese (Mn2+) under oxidative stress. Next, we identified a T6SS-4–dependent Mn2+-binding effector TseM, and its interacting partner MnoT, a Mn2+-specific TonB-dependent outer membrane transporter. Similar to the T6SS-4 genes, expression of mnoT is regulated by OxyR and is induced under oxidative stress and low Mn2+ conditions. Both TseM and MnoT are required for efficient uptake of Mn2+ across the outer membrane under Mn2+-limited and -oxidative stress conditions. The TseM–MnoT-mediated active Mn2+ transport system is also involved in contact-independent bacteria–bacteria competition and bacterial virulence. This finding provides a perspective for understanding the mechanisms of metal ion uptake and the roles of T6SS in bacteria–bacteria competition.

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Kulp, Adam, and Meta J. Kuehn. "Recognition of β-Strand Motifs by RseB Is Required for σEActivity in Escherichia coli." Journal of Bacteriology 193, no. 22 (September 9, 2011): 6179–86. http://dx.doi.org/10.1128/jb.05657-11.

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Gram-negative bacteria react to misfolded proteins in the envelope through a myriad of different stress response pathways. This cohort of pathways allows the bacteria to specifically respond to different types of damage, and many of these have been discovered to have key roles in the virulence of bacterial pathogens. Misfolded outer membrane proteins (OMPs) are typically recognized by the σEpathway, a highly conserved envelope stress response pathway. We examined the features of misfolded OMPs with respect to their ability to generate envelope stress responses. We determined that the secondary structure, particularly the potential to form β strands, is critical to inducing the σEresponse in an RseB-dependent manner. The sequence of the potential β-strand motif modulates the strength of the σEresponse generated by the constructs. By understanding the details of how such stress response pathways are activated, we can gain a greater understanding of how bacteria survive in harsh environments.

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WESCHE, ALISSA M., JOSHUA B. GURTLER, BRADLEY P. MARKS, and ELLIOT T. RYSER. "Stress, Sublethal Injury, Resuscitation, and Virulence of Bacterial Foodborne Pathogens†." Journal of Food Protection 72, no. 5 (May 1, 2009): 1121–38. http://dx.doi.org/10.4315/0362-028x-72.5.1121.

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Environmental stress and food preservation methods (e.g., heating, chilling, acidity, and alkalinity) are known to induce adaptive responses within the bacterial cell. Microorganisms that survive a given stress often gain resistance to that stress or other stresses via cross-protection. The physiological state of a bacterium is an important consideration when studying its response to food preservation techniques. This article reviews the various definitions of injury and stress, sublethal injury of bacteria, stresses that cause this injury, stress adaptation, cellular repair and response mechanisms, the role of reactive oxygen species in bacterial injury and resuscitation, and the potential for cross-protection and enhanced virulence as a result of various stress conditions.

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Wang, Tianwen, Chen Liang, Mengyuan Zheng, Lu Liu, Yafei An, Hongju Xu, Sa Xiao, and Lei Nie. "Ribosome Hibernation as a Stress Response of Bacteria." Protein & Peptide Letters 27, no. 11 (November 16, 2020): 1082–91. http://dx.doi.org/10.2174/0929866527666200610142118.

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Ribosome is primarily regarded as the committing organelle for the translation process. Besides the expansion of its function from a translational machine for protein synthesis to a regulatory platform for protein quality control, the activity regulation and recycling of ribosome have been deepened significantly. Recent advances have confirmed a novel mechanism in the regulation of ribosome activity when a cell encounters adverse conditions. Due to the binding of certain protein factors onto a ribosome, the structural and functional change of the ribosome inside the cell will take place, thereby leading to the formation of inactive ribosomes (70S monomer or 100S dimer), or ribosome hibernation. By ribosome hibernation, the overall protein synthesis rate of a cell could be slowed down. The resistance to adverse conditions or chemicals of the host cell will be enhanced. In this paper, we discussed the phenomenon, molecular mechanism, and physiological effect of ribosome hibernation when cells are under stresses. And then, we discussed the resuscitation of a hibernating ribosome and the role of ribosome hibernation in the treatment of antimicrobial infection.

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Jordan, Sina, Matthew I. Hutchings, and Thorsten Mascher. "Cell envelope stress response in Gram-positive bacteria." FEMS Microbiology Reviews 32, no. 1 (January 2008): 107–46. http://dx.doi.org/10.1111/j.1574-6976.2007.00091.x.

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Solioz, Marc, Helge K. Abicht, Mélanie Mermod, and Stefano Mancini. "Response of Gram-positive bacteria to copper stress." JBIC Journal of Biological Inorganic Chemistry 15, no. 1 (September 23, 2009): 3–14. http://dx.doi.org/10.1007/s00775-009-0588-3.

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Marles-Wright, Jon, and Richard J. Lewis. "Stress responses of bacteria." Current Opinion in Structural Biology 17, no. 6 (December 2007): 755–60. http://dx.doi.org/10.1016/j.sbi.2007.08.004.

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Porrini, Constance, Cyprien Guérin, Seav-Ly Tran, Rozenn Dervyn, Pierre Nicolas, and Nalini Ramarao. "Implication of a Key Region of Six Bacillus cereus Genes Involved in Siroheme Synthesis, Nitrite Reductase Production and Iron Cluster Repair in the Bacterial Response to Nitric Oxide Stress." International Journal of Molecular Sciences 22, no. 10 (May 11, 2021): 5079. http://dx.doi.org/10.3390/ijms22105079.

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Bacterial response to nitric oxide (NO) is of major importance for bacterial survival. NO stress is a main actor of the eukaryotic immune response and several pathogenic bacteria have developed means for detoxification and repair of the damages caused by NO. However, bacterial mechanisms of NO resistance by Gram-positive bacteria are poorly described. In the opportunistic foodborne pathogen Bacillus cereus, genome sequence analyses did not identify homologs to known NO reductases and transcriptional regulators, such as NsrR, which orchestrate the response to NO of other pathogenic or non-pathogenic bacteria. Using a transcriptomic approach, we investigated the adaptation of B. cereus to NO stress. A cluster of 6 genes was identified to be strongly up-regulated in the early phase of the response. This cluster contains an iron-sulfur cluster repair enzyme, a nitrite reductase and three enzymes involved in siroheme biosynthesis. The expression pattern and close genetic localization suggest a functional link between these genes, which may play a pivotal role in the resistance of B. cereus to NO stress during infection.

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Vrancken, Kristof, Lieve Van Mellaert, and Jozef Anné. "Characterization of the Streptomyces lividans PspA Response." Journal of Bacteriology 190, no. 10 (March 7, 2008): 3475–81. http://dx.doi.org/10.1128/jb.01966-07.

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ABSTRACT Phage shock protein (Psp) is induced by extracytoplasmic stress that may reduce the energy status of the cell. It is encoded in Escherichia coli by the phage shock protein regulon consisting of pspABCDE and by pspF and pspG. The phage shock protein system is highly conserved among a large number of gram-negative bacteria. However, many bacterial genomes contain only a pspA homologue but no homologues of the other genes of the Psp system. This conservation indicates that PspA alone might play an important role in these bacteria. In Streptomyces lividans, a soil-borne gram-positive bacterium, the phage shock protein system consists only of the pspA gene. In this report, we showed that pspA encodes a 28-kDa protein that is present in both the cytoplasmic and the membrane fractions of the S. lividans mycelium. We demonstrated that the pspA gene is strongly induced under stress conditions that attack membrane integrity and that it is essential for growth and survival under most of these conditions. The data reported here clearly show that PspA plays an important role in S. lividans under stress conditions despite the absence of other psp homologues, suggesting that PspA may be more important in most bacteria than previously thought.

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Wall, Judy D., Barbara J. Rapp-Giles, Merton F. Brown, and Jerry A. White. "Response of Desulfovibrio desulfuricans colonies to oxygen stress." Canadian Journal of Microbiology 36, no. 6 (June 1, 1990): 400–408. http://dx.doi.org/10.1139/m90-070.

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Oxygen tolerance of the strictly anaerobic sulfate-reducing bacteria is well documented and poorly understood. This capacity for surviving brief exposures to oxygen must be a major factor in the diversity of environmental niches observed for these bacteria. We observed that viable cells of Desulfovibrio desulfuricans (ATCC 27774) could be found in colonies on the surface of solidified medium exposed to air for periods as long as 1 month. During exposure to air, the originally black colonies became greyish white, presumably as a result of the air oxidation of the metal sulfide deposits. A black, brittle deposit formed at the bottom of the colony and, simultaneously, the colony descended into a dimple that developed into a well in the agar. Eventually the colony reached the bottom of the Petri dish. These changes did not take place when the colonies were maintained in an anaerobic chamber. The morphological changes took place with all strains tested: three strains of D. desulfuricans and one strain of Desulfovibrio gigas and Desulfovibrio multispirans. Continued sulfate reduction appeared to be essential. Cyclic sulfate (thiosulfate or sulfite) reduction to sulfide and reoxidation of sulfide by the oxygen in air are proposed to maintain the viability of the bacteria by providing substrates for energy production and by reducing oxygen tension. Scanning and transmission electron microscopy of colony and cellular changes are shown. Key words: Desulfovibrio, sulfate-reducing bacteria, oxygen tolerance, sulfate cycling, scanning electron microscopy.

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Soares Netto, Luis Eduardo. "Oxidative stress response in sugarcane." Genetics and Molecular Biology 24, no. 1-4 (December 2001): 93–102. http://dx.doi.org/10.1590/s1415-47572001000100014.

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Oxidative stress response in plants is still poorly understood in comparison with the correspondent phenomenon in bacteria, yeast and mammals. For instance, nitric oxide is assumed to play various roles in plants although no nitric oxide synthase gene has yet been isolated. This research reports the results of a search of the sugarcane expressed sequence tag (SUCEST) database for homologous sequences involved in the oxidative stress response. I have not found any gene similar to nitric oxide synthase in the SUCEST database although an alternative pathway for nitric oxide synthesis was proposed. I have also found several genes involved in antioxidant defense, e.g. metal chelators, low molecular weight compounds, antioxidant enzymes and repair systems. Ascorbate (vitamin C) is a key antioxidant in plants because it reaches high concentrations in cells and is a substrate for ascorbate peroxidase, an enzyme that I found in different isoforms in the SUCEST database. I also found many enzymes involved in the biosynthesis of low molecular weight antioxidants, which may be potential targets for genetic manipulation. The engineering of plants for increased vitamin C and E production may lead to improvements in the nutritional value and stress tolerance of sugarcane. The components of the antioxidant defense system interact and their synthesis is probably closely regulated. Transcription factors involved in regulation of the oxidative stress response in bacteria, yeast and mammals differ considerably among themselves and when I used them to search the SUCEST database only genes with weak similarities were found, suggesting that these transcription regulators are not very conserved. The involvement of reactive oxygen species and antioxidants in plant defense against pathogens is also discussed.

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Secor, Patrick R., Lia A. Michaels, Anina Ratjen, Laura K. Jennings, and Pradeep K. Singh. "Entropically driven aggregation of bacteria by host polymers promotes antibiotic tolerance inPseudomonas aeruginosa." Proceedings of the National Academy of Sciences 115, no. 42 (October 1, 2018): 10780–85. http://dx.doi.org/10.1073/pnas.1806005115.

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Bacteria causing chronic infections are generally observed living in cell aggregates suspended in polymer-rich host secretions, and bacterial phenotypes induced by aggregated growth may be key factors in chronic infection pathogenesis. Bacterial aggregation is commonly thought of as a consequence of biofilm formation; however the mechanisms producing aggregation in vivo remain unclear. Here we show that polymers that are abundant at chronic infection sites cause bacteria to aggregate by the depletion aggregation mechanism, which does not require biofilm formation functions. Depletion aggregation is mediated by entropic forces between uncharged or like-charged polymers and particles (e.g., bacteria). Our experiments also indicate that depletion aggregation of bacteria induces marked antibiotic tolerance that was dependent on the SOS response, a stress response activated by genotoxic stress. These findings raise the possibility that targeting conditions that promote depletion aggregation or mechanisms of depletion-mediated tolerance could lead to new therapeutic approaches to combat chronic bacterial infections.

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Alshareef, Manal H., Elizabeth L. Hartland, and Kathleen McCaffrey. "Effectors Targeting the Unfolded Protein Response during Intracellular Bacterial Infection." Microorganisms 9, no. 4 (March 29, 2021): 705. http://dx.doi.org/10.3390/microorganisms9040705.

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The unfolded protein response (UPR) is a homeostatic response to endoplasmic reticulum (ER) stress within eukaryotic cells. The UPR initiates transcriptional and post-transcriptional programs to resolve ER stress; or, if ER stress is severe or prolonged, initiates apoptosis. ER stress is a common feature of bacterial infection although the role of the UPR in host defense is only beginning to be understood. While the UPR is important for host defense against pore-forming toxins produced by some bacteria, other bacterial effector proteins hijack the UPR through the activity of translocated effector proteins that facilitate intracellular survival and proliferation. UPR-mediated apoptosis can limit bacterial replication but also often contributes to tissue damage and disease. Here, we discuss the dual nature of the UPR during infection and the implications of UPR activation or inhibition for inflammation and immunity as illustrated by different bacterial pathogens.

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da Cruz Nizer, Waleska Stephanie, Vasily Inkovskiy, Zoya Versey, Nikola Strempel, Edana Cassol, and Joerg Overhage. "Oxidative Stress Response in Pseudomonas aeruginosa." Pathogens 10, no. 9 (September 14, 2021): 1187. http://dx.doi.org/10.3390/pathogens10091187.

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Pseudomonas aeruginosa is a Gram-negative environmental and human opportunistic pathogen highly adapted to many different environmental conditions. It can cause a wide range of serious infections, including wounds, lungs, the urinary tract, and systemic infections. The high versatility and pathogenicity of this bacterium is attributed to its genomic complexity, the expression of several virulence factors, and its intrinsic resistance to various antimicrobials. However, to thrive and establish infection, P. aeruginosa must overcome several barriers. One of these barriers is the presence of oxidizing agents (e.g., hydrogen peroxide, superoxide, and hypochlorous acid) produced by the host immune system or that are commonly used as disinfectants in a variety of different environments including hospitals. These agents damage several cellular molecules and can cause cell death. Therefore, bacteria adapt to these harsh conditions by altering gene expression and eliciting several stress responses to survive under oxidative stress. Here, we used PubMed to evaluate the current knowledge on the oxidative stress responses adopted by P. aeruginosa. We will describe the genes that are often differently expressed under oxidative stress conditions, the pathways and proteins employed to sense and respond to oxidative stress, and how these changes in gene expression influence pathogenicity and the virulence of P. aeruginosa. Understanding these responses and changes in gene expression is critical to controlling bacterial pathogenicity and developing new therapeutic agents.

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Lagage, Valentine, and Stephan Uphoff. "Pulses and delays, anticipation and memory: seeing bacterial stress responses from a single-cell perspective." FEMS Microbiology Reviews 44, no. 5 (June 18, 2020): 565–71. http://dx.doi.org/10.1093/femsre/fuaa022.

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ABSTRACT Stress responses are crucial for bacteria to survive harmful conditions that they encounter in the environment. Although gene regulatory mechanisms underlying stress responses in bacteria have been thoroughly characterised for decades, recent advances in imaging technologies helped to uncover previously hidden dynamics and heterogeneity that become visible at the single-cell level. Despite the diversity of stress response mechanisms, certain dynamic regulatory features are frequently seen in single cells, such as pulses, delays, stress anticipation and memory effects. Often, these dynamics are highly variable across cells. While any individual cell may not achieve an optimal stress response, phenotypic diversity can provide a benefit at the population level. In this review, we highlight microscopy studies that offer novel insights into how bacteria sense stress, regulate protective mechanisms, cope with response delays and prepare for future environmental challenges. These studies showcase developments in the single-cell imaging toolbox including gene expression reporters, FRET, super-resolution microscopy and single-molecule tracking, as well as microfluidic techniques to manipulate cells and create defined stress conditions.

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Reichard, John F., Timothy P. Dalton, Howard G. Shertzer, and Alvaro Puga. "Induction of Oxidative Stress Responses by Dioxin and other Ligands of the Aryl Hydrocarbon Receptor." Dose-Response 3, no. 3 (May 1, 2005): dose—response.0. http://dx.doi.org/10.2203/dose-response.003.03.003.

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TCDD and other polyhalogenated aromatic hydrocarbon ligands of the aryl hydrocarbon receptor (AHR) have been classically considered as non-genotoxic compounds because they fail to be directly mutagenic in either bacteria or most in vitro assay systems. They do so in spite of having repeatedly been linked to oxidative stress and to mutagenic and carcinogenic outcomes. Oxidative stress, on the other hand, has been used as a marker for the toxicity of dioxin and its congeners. We have focused this review on the connection between oxidative stress induction and the toxic effects of fetal and adult dioxin exposure, with emphasis on the large species difference in sensitivity to this agent. We examine the roles that the dioxin-inducible cytochromes P450s play in the cellular and toxicological consequences of dioxin exposure with emphasis on oxidative stress involvement. Many components of the health consequences resulting from dioxin exposure may be attributable to epigenetic mechanisms arising from prolonged reactive oxygen generation.

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Konovalova, Anna, Jaclyn A. Schwalm, and Thomas J. Silhavy. "A Suppressor Mutation That Creates a Faster and More Robust σE Envelope Stress Response." Journal of Bacteriology 198, no. 17 (June 20, 2016): 2345–51. http://dx.doi.org/10.1128/jb.00340-16.

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ABSTRACTThe σE envelope stress response is an essential signal transduction pathway which detects and removes mistargeted outer membrane (OM) β-barrel proteins (OMPs) in the periplasm ofEscherichia coli. It relies on σE, an alternative sigma factor encoded by therpoEgene. Here we report a novel mutation, a nucleotide change of C to A in the third base of the second codon, which increases levels of σE (rpoE_S2R). TherpoE_S2Rmutation does not lead to the induction of the stress response during normal growth but instead changes the dynamics of induction upon periplasmic stress, resulting in a faster and more robust response. This allows cells to adapt faster to the periplasmic stress, avoiding lethal accumulation of unfolded OMPs in the periplasm caused by severe defects in the OMP assembly pathway.IMPORTANCESurvival of bacteria under conditions of external or internal stresses depends on timely induction of stress response signaling pathways to regulate expression of appropriate genes that function to maintain cellular homeostasis. Previous studies have shown that strong preinduction of envelope stress responses can allow bacteria to survive a number of lethal genetic perturbations. In our paper, we describe a unique mutation that enhances kinetics of the σE envelope stress response pathway rather than preinducing the response. This allows bacteria to quickly adapt to sudden and severe periplasmic stress.

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Cornelis, Pierre, Qing Wei, Simon C. Andrews, and Tiffany Vinckx. "Iron homeostasis and management of oxidative stress response in bacteria." Metallomics 3, no. 6 (2011): 540. http://dx.doi.org/10.1039/c1mt00022e.

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Chávez de Paz, L. E., G. Bergenholtz, G. Dahlén, and G. Svensäter. "Response to alkaline stress by root canal bacteria in biofilms." International Endodontic Journal 40, no. 5 (May 2007): 344–55. http://dx.doi.org/10.1111/j.1365-2591.2006.01226.x.

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Zhang, Ying, Dongfang Meng, Zhigang Wang, Huosheng Guo, and Yang Wang. "Oxidative stress response in two representative bacteria exposed to atrazine." FEMS Microbiology Letters 334, no. 2 (July 25, 2012): 95–101. http://dx.doi.org/10.1111/j.1574-6968.2012.02625.x.

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Spano, G., and S. Massa. "Environmental Stress Response in Wine Lactic Acid Bacteria: BeyondBacillus subtilis." Critical Reviews in Microbiology 32, no. 2 (January 2006): 77–86. http://dx.doi.org/10.1080/10408410600709800.

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Lushchak, Volodymyr I. "Adaptive response to oxidative stress: Bacteria, fungi, plants and animals." Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology 153, no. 2 (March 2011): 175–90. http://dx.doi.org/10.1016/j.cbpc.2010.10.004.

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Zhang, Ying, Dongfang Meng, Zhigang Wang, Huosheng Guo, Yang Wang, Xi Wang, and Xiaonan Dong. "Oxidative stress response in atrazine-degrading bacteria exposed to atrazine." Journal of Hazardous Materials 229-230 (August 2012): 434–38. http://dx.doi.org/10.1016/j.jhazmat.2012.05.054.

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da Cruz Nizer, Waleska Stephanie, Vasily Inkovskiy, and Joerg Overhage. "Surviving Reactive Chlorine Stress: Responses of Gram-Negative Bacteria to Hypochlorous Acid." Microorganisms 8, no. 8 (August 11, 2020): 1220. http://dx.doi.org/10.3390/microorganisms8081220.

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Sodium hypochlorite (NaOCl) and its active ingredient, hypochlorous acid (HOCl), are the most commonly used chlorine-based disinfectants. HOCl is a fast-acting and potent antimicrobial agent that interacts with several biomolecules, such as sulfur-containing amino acids, lipids, nucleic acids, and membrane components, causing severe cellular damage. It is also produced by the immune system as a first-line of defense against invading pathogens. In this review, we summarize the adaptive responses of Gram-negative bacteria to HOCl-induced stress and highlight the role of chaperone holdases (Hsp33, RidA, Cnox, and polyP) as an immediate response to HOCl stress. We also describe the three identified transcriptional regulators (HypT, RclR, and NemR) that specifically respond to HOCl. Besides the activation of chaperones and transcriptional regulators, the formation of biofilms has been described as an important adaptive response to several stressors, including HOCl. Although the knowledge on the molecular mechanisms involved in HOCl biofilm stimulation is limited, studies have shown that HOCl induces the formation of biofilms by causing conformational changes in membrane properties, overproducing the extracellular polymeric substance (EPS) matrix, and increasing the intracellular concentration of cyclic-di-GMP. In addition, acquisition and expression of antibiotic resistance genes, secretion of virulence factors and induction of the viable but nonculturable (VBNC) state has also been described as an adaptive response to HOCl. In general, the knowledge of how bacteria respond to HOCl stress has increased over time; however, the molecular mechanisms involved in this stress response is still in its infancy. A better understanding of these mechanisms could help understand host-pathogen interactions and target specific genes and molecules to control bacterial spread and colonization.

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Li, Tongda, Ross Mann, Jatinder Kaur, German Spangenberg, and Timothy Sawbridge. "Transcriptome Analyses of Barley Roots Inoculated with Novel Paenibacillus sp. and Erwinia gerundensis Strains Reveal Beneficial Early-Stage Plant–Bacteria Interactions." Plants 10, no. 9 (August 30, 2021): 1802. http://dx.doi.org/10.3390/plants10091802.

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Plant growth-promoting bacteria can improve host plant traits including nutrient uptake and metabolism and tolerance to biotic and abiotic stresses. Understanding the molecular basis of plant–bacteria interactions using dual RNA-seq analyses provides key knowledge of both host and bacteria simultaneously, leading to future enhancements of beneficial interactions. In this study, dual RNA-seq analyses were performed to provide insights into the early-stage interactions between barley seedlings and three novel bacterial strains (two Paenibacillus sp. strains and one Erwinia gerundensis strain) isolated from the perennial ryegrass seed microbiome. Differentially expressed bacterial and barley genes/transcripts involved in plant–bacteria interactions were identified, with varying species- and strain-specific responses. Overall, transcriptome profiles suggested that all three strains improved stress response, signal transduction, and nutrient uptake and metabolism of barley seedlings. Results also suggested potential improvements in seedling root growth via repressing ethylene biosynthesis in roots. Bacterial secondary metabolite gene clusters producing compounds that are potentially associated with interactions with the barley endophytic microbiome and associated with stress tolerance of plants under nutrient limiting conditions were also identified. The results of this study provided the molecular basis of plant growth-promoting activities of three novel bacterial strains in barley, laid a solid foundation for the future development of these three bacterial strains as biofertilisers, and identified key differences between bacterial strains of the same species in their responses to plants.

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Grace, Elicia D., Saumya Gopalkrishnan, Mary E. Girard, Matthew D. Blankschien, Wilma Ross, Richard L. Gourse, and Christophe Herman. "Activation of the σE-Dependent Stress Pathway by Conjugative TraR May Anticipate Conjugational Stress." Journal of Bacteriology 197, no. 5 (December 22, 2014): 924–31. http://dx.doi.org/10.1128/jb.02279-14.

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Horizontal gene transfer by conjugation plays a major role in bacterial evolution, allowing the acquisition of new traits, such as virulence and resistance to antibacterial agents. With the increased antibiotic resistance in bacterial pathogens, a better understanding of how bacteria modulate conjugation under changing environments and the genetic factors involved is needed. Despite the evolutionary advantages conjugation may confer, the process can be quite stressful for the donor cell. Here, we characterize the ability of TraR, encoded on the episomal F′ plasmid, to upregulate the σEextracytoplasmic stress pathway inEscherichia coli. TraR, a DksA homolog, modulates transcription initiation through the secondary channel of RNA polymerase. We show here that TraR activates transcription directly; however, unlike DksA, it does so without using ppGpp as a cofactor. TraR expression can stimulate the σEextracytoplasmic stress response independently of the DegS/RseA signal transduction cascade. In the absence of TraR, bacteria carrying conjugative plasmids become more susceptible to external stress. We propose that TraR increases the concentrations of periplasmic chaperones and proteases by directly activating the transcription of σE-dependent promoters; this increased protein folding capacity may prepare the bacterium to endure the periplasmic stress of sex pilus biosynthesis during mating.

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Ortiz de Orué Lucana, Darío, Ina Wedderhoff, and Matthew R. Groves. "ROS-Mediated Signalling in Bacteria: Zinc-Containing Cys-X-X-Cys Redox Centres and Iron-Based Oxidative Stress." Journal of Signal Transduction 2012 (September 29, 2012): 1–9. http://dx.doi.org/10.1155/2012/605905.

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Bacteria are permanently in contact with reactive oxygen species (ROS), both over the course of their life cycle as well that present in their environment. These species cause damage to proteins, lipids, and nucleotides, negatively impacting the organism. To detect these ROS molecules and to stimulate the expression of proteins involved in antioxidative stress response, bacteria use a number of different protein-based regulatory and sensory systems. ROS-based stress detection mechanisms induce posttranslational modifications, resulting in overall conformational and structural changes within sensory proteins. The subsequent structural rearrangements result in changes of protein activity, which lead to regulated and appropriate response on the transcriptional level. Many bacterial enzymes and regulatory proteins possess a conserved signature, the zinc-containing redox centre Cys-X-X-Cys in which a disulfide bridge is formed upon oxidative stress. Other metal-dependent oxidative modifications of amino acid side-chains (dityrosines, 2-oxo-histidines, or carbonylation) also modulate the activity of redox-sensitive proteins. Using molecular biology, biochemistry, biophysical, and structure biology tools, molecular mechanisms involved in sensing and response to oxidative stress have been elucidated in detail. In this review, we analyze some examples of bacterial redox-sensing proteins involved in antioxidative stress response and focus further on the currently known molecular mechanism of function.

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Panoff, Jean-Michel, Bouachanh Thammavongs, Micheline Guéguen, and Philippe Boutibonnes. "Cold Stress Responses in Mesophilic Bacteria." Cryobiology 36, no. 2 (March 1998): 75–83. http://dx.doi.org/10.1006/cryo.1997.2069.

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Wu, Pengyu, Qiuyan Zhu, Rui Yang, Yuxia Mei, Zhenmin Chen, and Yunxiang Liang. "Differences in Acid Stress Response of Lacticaseibacillus paracasei Zhang Cultured from Solid-State Fermentation and Liquid-State Fermentation." Microorganisms 9, no. 9 (September 14, 2021): 1951. http://dx.doi.org/10.3390/microorganisms9091951.

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Liquid-state fermentation (LSF) and solid-state fermentation (SSF) are two forms of industrial production of lactic acid bacteria (LAB). The choice of two fermentations for LAB production has drawn wide concern. In this study, the tolerance of bacteria produced by the two fermentation methods to acid stress was compared, and the reasons for the tolerance differences were analyzed at the physiological and transcriptional levels. The survival rate of the bacterial agent obtained from solid-state fermentation was significantly higher than that of bacteria obtained from liquid-state fermentation after spray drying and cold air drying. However, the tolerance of bacterial cells obtained from liquid-state fermentation to acid stress was significantly higher than that from solid-state fermentation. The analysis at physiological level indicated that under acid stress, cells from liquid-state fermentation displayed a more solid and complete membrane structure, higher cell membrane saturated fatty acid, more stable intracellular pH, and more stable activity of ATPase and glutathione reductase, compared with cells from solid-state fermentation, and these physiological differences led to better tolerance to acid stress. In addition, transcriptomic analysis showed that in the cells cultured from liquid-state fermentation, the genes related to glycolysis, inositol phosphate metabolism, and carbohydrate transport were down-regulated, whereas the genes related to fatty acid synthesis and glutamate metabolism were upregulated, compared with those in cells from solid-state fermentation. In addition, some genes related to acid stress response such as cspA, rimP, rbfA, mazF, and nagB were up-regulated. These findings provide a new perspective for the study of acid stress tolerance of L. paracasei Zhang and offer a reference for the selection of fermentation methods of LAB production.

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Rieder, Ronald J., Zhihui Zhao, and Boris Zavizion. "New Approach for Drug Susceptibility Testing: Monitoring the Stress Response of Mycobacteria." Antimicrobial Agents and Chemotherapy 53, no. 11 (August 24, 2009): 4598–603. http://dx.doi.org/10.1128/aac.00643-09.

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ABSTRACT Methods currently used for in vitro drug susceptibility testing are based on the assessment of bacterial growth-related processes. This reliance on cellular reproduction leads to prolonged incubation times, particularly for slowly growing organisms such as mycobacteria. A new rapid phenotypic method for the drug susceptibility testing of mycobacteria is described. The method is based on the detection of the physiological stress developed by susceptible mycobacterial cells in the presence of an antimicrobial compound. The induced stress was quantified by differential monitoring of the dielectric properties of the bacterial suspension, an easily measurable electronic property. The data presented here characterize the stress developed by Mycobacterium tuberculosis cells treated with rifampin (rifampicin), isoniazid, ethambutol, and pyrazinamide. Changes in the dielectric-based profiles of the drug-treated bacteria revealed the respective susceptibilities in near real time, and the susceptibilities were well correlated with conventional susceptibility test data.

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Parmely, Michael J., Fuan Wang, and Douglas Wright. "Gamma Interferon Prevents the Inhibitory Effects of Oxidative Stress on Host Responses to Escherichia coliInfection." Infection and Immunity 69, no. 4 (April 1, 2001): 2621–29. http://dx.doi.org/10.1128/iai.69.4.2621-2629.2001.

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ABSTRACT Oxidative stress occurs in animals challenged with bacterial endotoxin and can affect the expression of important host inflammatory genes. However, much less is known about the effects of oxidative stress on responses to gram-negative bacteria. The current study compared the effects of redox imbalance on hepatic responses of mice to Escherichia coli bacteria versus purified endotoxic lipopolysaccharide (LPS). Oxidative stress induced by glutathione depletion virtually eliminated hepatic tumor necrosis factor alpha responses to both E. coli and LPS. Inducible NO synthase (iNOS) and intercellular adhesion molecule-1 (ICAM-1) expression was also markedly inhibited by glutathione depletion in LPS-challenged mice, but was unaffected in E. coli-infected animals. Three findings suggested that gamma interferon (IFN-γ) production explained the differences between LPS and bacterial challenge. Glutathione depletion completely inhibited the IFN-γ response to LPS, but only partially inhibited IFN-γ production in infected mice. Exogenous IFN-γ restored iNOS and ICAM-1 responses to LPS in stressed mice. Conversely, IFN-γ-deficient, glutathione-depleted mice showed a marked decrease in iNOS and ICAM-1 expression when challenged with E. coli. These findings indicate that both the nature of the microbial challenge and the production of IFN-γ can be important in determining the effects of redox imbalance during gram-negative bacterial infections.

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SAIDI, Abbas, Zohreh HAJIBARAT, and Zahra HAJIBARAT. "Identification of responsive genes and analysis of genes with bacterial-inducible cis-regulatory elements in the promoter regions in Oryza sativa L." Acta agriculturae Slovenica 116, no. 1 (September 25, 2020): 115. http://dx.doi.org/10.14720/aas.2020.116.1.1035.

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Bacterial blight of rice caused by Xanthomonas oryzae pv. oryzae (Xoo) is one of the most critical diseases in rice. In order to study rice responsive genes to bacterial stress, microarray data were retrieved from GEO dataset. To identify the responsive genes to biotic stress (bacteria) bioinformatic tools were employed and the data presented in the forms of heatmap, gene ontology, gene network, and cis-element prediction were used. Almost all responsive genes were down-regulated at around 3 h time point and up-regulated 24 h time point in response to bacterial stress in rice varieties (Oryza sativa subs. japonica ‘IR64’, ‘IRBB5’, ‘IRBB7’ and ‘Y73’). Gene ontology showed that genes are involved in different biological processes including translation and cellular protein metabolic processes. Network analysis showed that genes expressed in response to pathogen infection (Xoo) included protein translation, eukaryotic initiation factors (eIFs), ribosomal proteins, protein ubiquitin, and MAPK genes. The genes expressed in response to bacterial stress can enable plant balance between synthesis and degradation of proteins which in turn allows plants for further growth and development. TATA-box and CAAT box had the highest number of cis elements involved in bacterial stress. These genes can provide novel insights into regulatory mechanisms in biotic stress responses in rice. Identification of bacterial stress response/tolerance genes of rice can assist the molecular breeding of new rice varieties tolerant to bacterial stress.

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KALBURGE, SAI SIDDARTH, W. BRIAN WHITAKER, and E. FIDELMA BOYD. "High-Salt Preadaptation of Vibrio parahaemolyticus Enhances Survival in Response to Lethal Environmental Stresses." Journal of Food Protection 77, no. 2 (February 1, 2014): 246–53. http://dx.doi.org/10.4315/0362-028x.jfp-13-241.

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Adaptation to changing environmental conditions is an important strategy for survival of foodborne bacterial pathogens. Vibrio parahaemolyticus is a gram-negative seafoodborne enteric pathogen found in the marine environment both free living and associated with oysters. This pathogen is a moderate halophile, with optimal growth at 3% NaCl. Among the several stresses imposed upon enteric bacteria, acid stress is perhaps one of the most important. V. parahaemolyticus has a lysine decarboxylase system responsible for decarboxylation of lysine to the basic product cadaverine, an important acid stress response system in bacteria. Preadaptation to mild acid conditions, i.e., the acid tolerance response, enhances survival under lethal acid conditions. Because of the variety of conditions encountered by V. parahaemolyticus in the marine environment and in oyster postharvest facilities, we examined the nature of the V. parahaemolyticus acid tolerance response under high-salinity conditions. Short preadaptation to a 6% salt concentration increased survival of the wild-type strain but not that of a cadA mutant under lethal acid conditions. However, prolonged exposure to high salinity (16 h) increased survival of both the wild-type and the cadA mutant strains. This phenotype was not dependent on the stress response sigma factor RpoS. Although this preadaptation response is much more pronounced in V. parahaemolyticus, this characteristic is not limited to this species. Both Vibrio cholerae and Vibrio vulnificus also survive better under lethal acid stress conditions when preadapted to high-salinity conditions. High salt both protected the organism against acid stress and increased survival under −20°C cold stress conditions. High-salt adaptation of V. parahaemolyticus strains significantly increases survival under environmental stresses that would otherwise be lethal to these bacteria.

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Ong, Cheryl-Lynn Y., Adam J. Potter, Claudia Trappetti, Mark J. Walker, Michael P. Jennings, James C. Paton, and Alastair G. McEwan. "Interplay between Manganese and Iron in Pneumococcal Pathogenesis: Role of the Orphan Response Regulator RitR." Infection and Immunity 81, no. 2 (November 26, 2012): 421–29. http://dx.doi.org/10.1128/iai.00805-12.

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ABSTRACTStreptococcus pneumoniae(the pneumococcus) is a major human pathogen that is carried asymptomatically in the nasopharynx by up to 70% of the human population. Translocation of the bacteria into internal sites can cause a range of diseases, such as pneumonia, otitis media, meningitis, and bacteremia. This transition from nasopharynx to growth at systemic sites means that the pneumococcus needs to adjust to a variety of environmental conditions, including transition metal ion availability. Although it is an important nutrient, iron potentiates oxidative stress, and it is established that inS. pneumoniae, expression of iron transport systems and proteins that protect against oxidative stress are regulated by an orphan response regulator, RitR. In this study, we investigated the effect of iron and manganese ion availability on the growth of aritRmutant. Deletion ofritRled to impaired growth of bacteria in high-iron medium, but this phenotype could be suppressed with the addition of manganese. Measurement of metal ion accumulation indicated that manganese prevents iron accumulation. Furthermore, the addition of manganese also led to a reduction in the amount of hydrogen peroxide produced by bacterial cells. Studies of virulence in a murine model of infection indicated that RitR was not essential for pneumococcal survival and suggested that derepression of iron uptake systems may enhance the survival of pneumococci in some niches.

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Leonard, Cory Ann, Frederic Dewez, and Nicole Borel. "Penicillin G-Induced Chlamydial Stress Response in a Porcine Strain ofChlamydia pecorum." International Journal of Microbiology 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/3832917.

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Chlamydia pecorumcauses asymptomatic infection and pathology in ruminants, pigs, and koalas. We characterized the antichlamydial effect of the beta lactam penicillin G onChlamydia pecorumstrain 1710S (porcine abortion isolate). Penicillin-exposed and mock-exposed infected host cells showed equivalent inclusions numbers. Penicillin-exposed inclusions contained aberrant bacterial forms and exhibited reduced infectivity, while mock-exposed inclusions contained normal bacterial forms and exhibited robust infectivity. Infectious bacteria production increased upon discontinuation of penicillin exposure, compared to continued exposure.Chlamydia-induced cell death occurred in mock-exposed controls; cell survival was improved in penicillin-exposed infected groups. Similar results were obtained both in the presence and in the absence of the eukaryotic protein translation inhibitor cycloheximide and at different times of initiation of penicillin exposure. These data demonstrate that penicillin G induces the chlamydial stress response (persistence) and is not bactericidal, for this chlamydial species/strainin vitro, regardless of host cellde novoprotein synthesis.

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Lippmann, Juliane, Frederik Gwinner, Camille Rey, Uyanga Tamir, Helen K. W. Law, Benno Schwikowski, and Jost Enninga. "Bacterial Internalization, Localization, and Effectors Shape the Epithelial Immune Response during Shigella flexneri Infection." Infection and Immunity 83, no. 9 (June 29, 2015): 3624–37. http://dx.doi.org/10.1128/iai.00574-15.

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Intracellular pathogens are differentially sensed by the compartmentalized host immune system. Nevertheless, gene expression studies of infected cells commonly average the immune responses, neglecting the precise pathogen localization. To overcome this limitation, we dissected the transcriptional immune response toShigella flexneriacross different infection stages in bulk and single cells. This identified six distinct transcriptional profiles characterizing the dynamic, multilayered host response in both bystander and infected cells. These profiles were regulated by external and internal danger signals, as well as whether bacteria were membrane bound or cytosolic. We found that bacterial internalization triggers a complex, effector-independent response in bystander cells, possibly to compensate for the undermined host gene expression in infected cells caused by bacterial effectors, particularly OspF. Single-cell analysis revealed an important bacterial strategy to subvert host responses in infected cells, demonstrating that OspF disrupts concomitant gene expression of proinflammatory, apoptosis, and stress pathways within cells. This study points to novel mechanisms through which bacterial internalization, localization, and injected effectors orchestrate immune response transcriptional signatures.

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Lemmens, Liesbeth, Rani Baes, and Eveline Peeters. "Heat shock response in archaea." Emerging Topics in Life Sciences 2, no. 4 (November 22, 2018): 581–93. http://dx.doi.org/10.1042/etls20180024.

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An adequate response to a sudden temperature rise is crucial for cellular fitness and survival. While heat shock response (HSR) is well described in bacteria and eukaryotes, much less information is available for archaea, of which many characterized species are extremophiles thriving in habitats typified by large temperature gradients. Here, we describe known molecular aspects of archaeal heat shock proteins (HSPs) as key components of the protein homeostasis machinery and place this in a phylogenetic perspective with respect to bacterial and eukaryotic HSPs. Particular emphasis is placed on structure–function details of the archaeal thermosome, which is a major element of the HSR and of which subunit composition is altered in response to temperature changes. In contrast with the structural response, it is largely unclear how archaeal cells sense temperature fluctuations and which molecular mechanisms underlie the corresponding regulation. We frame this gap in knowledge by discussing emerging questions related to archaeal HSR and by proposing methodologies to address them. Additionally, as has been shown in bacteria and eukaryotes, HSR is expected to be relevant for the control of physiology and growth in various stress conditions beyond temperature stress. A better understanding of this essential cellular process in archaea will not only provide insights into the evolution of HSR and of its sensing and regulation, but also inspire the development of biotechnological applications, by enabling transfer of archaeal heat shock components to other biological systems and for the engineering of archaea as robust cell factories.

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Holmqvist, Erik, and E. Gerhart H. Wagner. "Impact of bacterial sRNAs in stress responses." Biochemical Society Transactions 45, no. 6 (November 3, 2017): 1203–12. http://dx.doi.org/10.1042/bst20160363.

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Bacterial life is harsh and involves numerous environmental and internal challenges that are perceived as stresses. Consequently, adequate responses to survive, cope with, and counteract stress conditions have evolved. In the last few decades, a class of small, non-coding RNAs (sRNAs) has been shown to be involved as key players in stress responses. This review will discuss — primarily from an enterobacterial perspective — selected stress response pathways that involve antisense-type sRNAs. These include themes of how bacteria deal with severe envelope stress, threats of DNA damage, problems with poisoning due to toxic sugar intermediates, issues of iron homeostasis, and nutrient limitation/starvation. The examples discussed highlight how stress relief can be achieved, and how sRNAs act mechanistically in regulatory circuits. For some cases, we will propose scenarios that may suggest why contributions from post-transcriptional control by sRNAs, rather than transcriptional control alone, appear to be a beneficial and universally selected feature.

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Fourie, Kezia R., and Heather L. Wilson. "Understanding GroEL and DnaK Stress Response Proteins as Antigens for Bacterial Diseases." Vaccines 8, no. 4 (December 17, 2020): 773. http://dx.doi.org/10.3390/vaccines8040773.

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Bacteria do not simply express a constitutive panel of proteins but they instead undergo dynamic changes in their protein repertoire in response to changes in nutritional status and when exposed to different environments. These differentially expressed proteins may be suitable to use for vaccine antigens if they are virulence factors. Immediately upon entry into the host organism, bacteria are exposed to a different environment, which includes changes in temperature, osmotic pressure, pH, etc. Even when an organism has already penetrated the blood or lymphatics and it then enters another organ or a cell, it can respond to these new conditions by increasing the expression of virulence factors to aid in bacterial adherence, invasion, or immune evasion. Stress response proteins such as heat shock proteins and chaperones are some of the proteins that undergo changes in levels of expression and/or changes in cellular localization from the cytosol to the cell surface or the secretome, making them potential immunogens for vaccine development. Herein we highlight literature showing that intracellular chaperone proteins GroEL and DnaK, which were originally identified as playing a role in protein folding, are relocated to the cell surface or are secreted during invasion and therefore may be recognized by the host immune system as antigens. In addition, we highlight literature showcasing the immunomodulation effects these proteins can have on the immune system, also making them potential adjuvants or immunotherapeutics.

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Okamoto, Susumu, and Hiromi Kameya. "Antibacterial Action of Acid Preservatives and Acid Stress Response in Bacteria." Nippon Shokuhin Kagaku Kogaku Kaishi 65, no. 3 (2018): 148–53. http://dx.doi.org/10.3136/nskkk.65.148.

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Hecker, Michael, Jan Pané-Farré, and Völker Uwe. "SigB-Dependent General Stress Response inBacillus subtilisand Related Gram-Positive Bacteria." Annual Review of Microbiology 61, no. 1 (October 2007): 215–36. http://dx.doi.org/10.1146/annurev.micro.61.080706.093445.

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YAMAMOTO, Tomoko. "Regulatory mechanisms for stress response and pathogenesis of facultative intracellular bacteria." Nippon Saikingaku Zasshi 66, no. 4 (2011): 517–29. http://dx.doi.org/10.3412/jsb.66.517.

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Sun, Jiaqi, and Yaoyu Bai. "Predator-induced stress influences fall armyworm immune response to inoculating bacteria." Journal of Invertebrate Pathology 172 (May 2020): 107352. http://dx.doi.org/10.1016/j.jip.2020.107352.

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Fu, Huihui, Jie Yuan, and Haichun Gao. "Microbial oxidative stress response: Novel insights from environmental facultative anaerobic bacteria." Archives of Biochemistry and Biophysics 584 (October 2015): 28–35. http://dx.doi.org/10.1016/j.abb.2015.08.012.

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Swenson, Gabriel J., J. Stochastic, Franklyn F. Bolander, and Richard A. Long. "Acid stress response in environmental and clinical strains of enteric bacteria." Frontiers in Biology 7, no. 6 (March 31, 2012): 495–505. http://dx.doi.org/10.1007/s11515-012-1191-5.

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Journal articles on the topic 'Stress response of bacteria'

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