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      The role of bacterial signaling networks in antibiotics response and resistance regulation


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          Excessive use of antibiotics poses a threat to public health and the environment. In ecosystems, such as the marine environment, antibiotic contamination has led to an increase in bacterial resistance. Therefore, the study of bacterial response to antibiotics and the regulation of resistance formation have become an important research field. Traditionally, the processes related to antibiotic responses and resistance regulation have mainly included the activation of efflux pumps, mutation of antibiotic targets, production of biofilms, and production of inactivated or passivation enzymes. In recent years, studies have shown that bacterial signaling networks can affect antibiotic responses and resistance regulation. Signaling systems mostly alter resistance by regulating biofilms, efflux pumps, and mobile genetic elements. Here we provide an overview of how bacterial intraspecific and interspecific signaling networks affect the response to environmental antibiotics. In doing so, this review provides theoretical support for inhibiting bacterial antibiotic resistance and alleviating health and ecological problems caused by antibiotic contamination.

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          Bacterial quorum-sensing network architectures.

          Quorum sensing is a cell-cell communication process in which bacteria use the production and detection of extracellular chemicals called autoinducers to monitor cell population density. Quorum sensing allows bacteria to synchronize the gene expression of the group, and thus act in unison. Here, we review the mechanisms involved in quorum sensing with a focus on the Vibrio harveyi and Vibrio cholerae quorum-sensing systems. We discuss the differences between these two quorum-sensing systems and the differences between them and other paradigmatic bacterial signal transduction systems. We argue that the Vibrio quorum-sensing systems are optimally designed to precisely translate extracellular autoinducer information into internal changes in gene expression. We describe how studies of the V. harveyi and V. cholerae quorum-sensing systems have revealed some of the fundamental mechanisms underpinning the evolution of collective behaviors.
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            Structural identification of a bacterial quorum-sensing signal containing boron.

            Cell-cell communication in bacteria is accomplished through the exchange of extracellular signalling molecules called autoinducers. This process, termed quorum sensing, allows bacterial populations to coordinate gene expression. Community cooperation probably enhances the effectiveness of processes such as bioluminescence, virulence factor expression, antibiotic production and biofilm development. Unlike other autoinducers, which are specific to a particular species of bacteria, a recently discovered autoinducer (AI-2) is produced by a large number of bacterial species. AI-2 has been proposed to serve as a 'universal' signal for inter-species communication. The chemical identity of AI-2 has, however, proved elusive. Here we present the crystal structure of an AI-2 sensor protein, LuxP, in a complex with autoinducer. The bound ligand is a furanosyl borate diester that bears no resemblance to previously characterized autoinducers. Our findings suggest that addition of naturally occurring borate to an AI-2 precursor generates active AI-2. Furthermore, they indicate a potential biological role for boron, an element required by a number of organisms but for unknown reasons.
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              Exploiting quorum sensing to confuse bacterial pathogens.

              Cell-cell communication, or quorum sensing, is a widespread phenomenon in bacteria that is used to coordinate gene expression among local populations. Its use by bacterial pathogens to regulate genes that promote invasion, defense, and spread has been particularly well documented. With the ongoing emergence of antibiotic-resistant pathogens, there is a current need for development of alternative therapeutic strategies. An antivirulence approach by which quorum sensing is impeded has caught on as a viable means to manipulate bacterial processes, especially pathogenic traits that are harmful to human and animal health and agricultural productivity. The identification and development of chemical compounds and enzymes that facilitate quorum-sensing inhibition (QSI) by targeting signaling molecules, signal biogenesis, or signal detection are reviewed here. Overall, the evidence suggests that QSI therapy may be efficacious against some, but not necessarily all, bacterial pathogens, and several failures and ongoing concerns that may steer future studies in productive directions are discussed. Nevertheless, various QSI successes have rightfully perpetuated excitement surrounding new potential therapies, and this review highlights promising QSI leads in disrupting pathogenesis in both plants and animals.

                Author and article information

                Mar Life Sci Technol
                Mar Life Sci Technol
                Marine Life Science & Technology
                Springer Nature Singapore (Singapore )
                28 March 2022
                28 March 2022
                May 2022
                : 4
                : 2
                : 163-178
                [1 ]GRID grid.4422.0, ISNI 0000 0001 2152 3263, College of Marine Life Sciences, , Ocean University of China, ; Qingdao, 266003 China
                [2 ]GRID grid.4422.0, ISNI 0000 0001 2152 3263, Institute of Evolution and Marine Biodiversity, , Ocean University of China, ; Qingdao, 266003 China
                [3 ]Laboratory for Marine Ecology and Environmental Science, National Laboratory for Marine Science and Technology (Qingdao), Qingdao, 266071 China
                © The Author(s) 2022

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                : 25 August 2021
                : 7 January 2022
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                © Ocean University of China 2022

                bacterial antibiotic resistance,ahl,ai-2,aip,indole,dsf
                bacterial antibiotic resistance, ahl, ai-2, aip, indole, dsf


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