Bibliografie tematiche / Quorum sensing

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Letteratura scientifica selezionata sul tema "Quorum sensing"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 9 giugno 2025

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Articoli di riviste sul tema "Quorum sensing"

Sahu, Dr Babita, Dr Srikanth Guduguntla, Dr Sachin B. Mangalekar, Dr Sunaina Shetty, Dr Priyanka Thakur, and Dr Supriya Mishra. "Quorum Sensing and Quorum Quenching Facebook of Microbial World." International Journal of Scientific Research 3, no. 2 (June 1, 2012): 423–26. http://dx.doi.org/10.15373/22778179/feb2014/139.

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Hentzer, Morten, Leo Eberl, John Nielsen, and Michael Givskov. "Quorum Sensing." BioDrugs 17, no. 4 (2003): 241–50. http://dx.doi.org/10.2165/00063030-200317040-00003.

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Marshall, J. "Quorum sensing." Proceedings of the National Academy of Sciences 110, no. 8 (February 1, 2013): 2690. http://dx.doi.org/10.1073/pnas.1301432110.

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Lal, Avantika. "Quorum sensing." Resonance 14, no. 9 (September 2009): 866–71. http://dx.doi.org/10.1007/s12045-009-0082-9.

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Williams, Paul. "Quorum sensing." International Journal of Medical Microbiology 296, no. 2-3 (April 2006): 57–59. http://dx.doi.org/10.1016/j.ijmm.2006.01.034.

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Wackett, Lawrence P. "Quorum sensing." Environmental Microbiology 10, no. 10 (September 10, 2008): 2899–900. http://dx.doi.org/10.1111/j.1462-2920.2008.01755.x.

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Diggle, Stephen P., Shanika A. Crusz, and Miguel Cámara. "Quorum sensing." Current Biology 17, no. 21 (November 2007): R907—R910. http://dx.doi.org/10.1016/j.cub.2007.08.045.

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YUAN, ZongHui, ZhenLi LIU, MengHong DAI, HaiHong HAO, and GuYue CHENG. "Quorum sensing of pathogenic bacteria and quorum-sensing inhibitors." Chinese Science Bulletin 57, no. 21 (July 1, 2012): 1964–77. http://dx.doi.org/10.1360/972011-2465.

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Krom, Bastiaan P., Niva Levy, Michael M. Meijler, and Mary Ann Jabra-Rizk. "Farnesol andCandida albicans: Quorum Sensing or Not Quorum Sensing?" Israel Journal of Chemistry 56, no. 5 (July 21, 2015): 295–301. http://dx.doi.org/10.1002/ijch.201500025.

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Wright, Patricia P., and Srinivas Sulugodu Ramachandra. "Quorum Sensing and Quorum Quenching with a Focus on Cariogenic and Periodontopathic Oral Biofilms." Microorganisms 10, no. 9 (September 3, 2022): 1783. http://dx.doi.org/10.3390/microorganisms10091783.

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Abstract (sommario):

Numerous in vitro studies highlight the role of quorum sensing in the pathogenicity and virulence of biofilms. This narrative review discusses general principles in quorum sensing, including Gram-positive and Gram-negative models and the influence of flow, before focusing on quorum sensing and quorum quenching in cariogenic and periodontopathic biofilms. In cariology, quorum sensing centres on the role of Streptococcus mutans, and to a lesser extent Candida albicans, while Fusobacterium nucleatum and the red complex pathogens form the basis of the majority of the quorum sensing research on periodontopathic biofilms. Recent research highlights developments in quorum quenching, also known as quorum sensing inhibition, as a potential antimicrobial tool to attenuate the pathogenicity of oral biofilms by the inhibition of bacterial signalling networks. Quorum quenchers may be synthetic or derived from plant or bacterial products, or human saliva. Furthermore, biofilm inhibition by coating quorum sensing inhibitors on dental implant surfaces provides another potential application of quorum quenching technologies in dentistry. While the body of predominantly in vitro research presented here is steadily growing, the clinical value of quorum sensing inhibitors against in vivo oral polymicrobial biofilms needs to be ascertained.

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Tesi sul tema "Quorum sensing"

Pereira, Daniel Albuquerque. "Quorum sensing em cianobactérias." Universidade Federal de Minas Gerais, 2014. http://hdl.handle.net/1843/BUOS-9NFKZN.

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The terminology quorum sensing is used to identify a cellular communication phenomenon in the bacterial domain, which happens when a bacteria population reaches a defined cellular density. During the activation of the phenomenon changes in the expression of several genes and consequently in the physiology of the cell are triggered. Concerning cyanobacteria, there is a lack of information about quorum sensing. Some studies show that quorum sensing inducer compounds may alter physiological characteristics of certain cyanobacteria strains. Besides that, indirect evidences have shown that cellular density may influence microcystin production. The capacity to form blooms in certain conditions is also an important characteristic found in the cyanobacteria group. In these conditions the cellular density of a population may reach elevated numbers, consisting of an ideal scenario for quorum sensing. There are a remarkably number of studies regarding cyanobacterial blooms, but little is known about what happens with a population at molecular and physiological levels. The aim of this study was to characterize four strains of cyanobacteria regarding the production of peptides and to use these strains in experiments with the objective of investigating evidences of quorum sensing system in cyanobacteria and its connection with the synthesis of oligopeptides. In order to fulfill these objectives biochemical and molecular techniques were used. The results obtained showed that the production of oligopeptides is affected by cellular density, being, in most cases, higher in situations with an elevated number of cells. It was demonstrated by real time PCR that acylhomoserine lactone autoinducers (AHLs), which are responsible for the activation of the quorum sensing in various groups of gram-negative bacteria, affect the transcription of genes linked to the production of microcystins, cyanopeptolins and microviridins. Through ELISA assays it was also seen that AHLs affect the microcystin production in the same pattern in which they affect the transcription of genes connected to its synthesis. With this work it was observed that cellular density and possibly quorum sensing are key factors in secondary metabolite synthesis in cyanobacteria and should be considered when studying these compounds and their connection with the environment.<br>O termo quorum sensing refere-se a um fenômeno de comunicação celular existente em bactérias, onde ao se atingir uma certa densidade populacional mudanças no padrão de expressão gênica, e consequentemente da fisiologia das células são disparadas. No que diz respeito a cianobactérias, poucos trabalhos com enfoque em quorum sensing foram realizados. Alguns estudos mostram que substâncias indutoras de quorum sensing podem alterar algumas características fisiológicas de algumas cepas de cianobactérias. Evidências indiretas mostraram que a diferença na densidade celular pode afetar a produção de microcistinas. A capacidade de produzir florações em determinadas condições é outro aspecto importante das cianobactérias. Nestas situações a densidade populacional das espécies dominantes atinge valores muito altos, podendo constituir uma situação ideal para a ocorrência do quorum sensing. Existem diversos estudos sobre florações, no entanto pouco se sabe sobre o que ocorre com as populações de cianobactérias em nivel molecular e também fisiológico. Este trabalho teve o objetivo de caracterizar quatro cepas de cianobactérias quanto à produção de peptídeos e utilizá-las em experimentos com a finalidade de encontrar evidências da existência de quorum sensing em cianobactérias e sua relação com a produção de oligopeptídeos. Para cumprir estes objetivos foram utilizadas técnicas de bioquímica e biologia molecular. Os resultados encontrados demonstraram que a produção de oligopeptídeos é afetada pela densidade celular, sendo, na maioria dos casos, maior nas situações com alto número de células. Foi verificado através de PCR em tempo real que auto indutores do tipo acil-homoserina lactonas (AHLs), responsáveis pela ativação do quorum sensing em diversos grupos de bactérias gram-negativas, afetam a transcrição de genes ligados a produção dos peptídeos microcistina, cianopeptolina e microviridina. Através de testes de ELISA foi visto também que as AHLs afetam a produção de microcistinas da mesma forma que influenciam a transcrição dos genes liagados à sua síntese. Com este trabalho foi visto que densidade celular e, possivelmente, quorum sensing são fatores importantes na síntese de metabólitos secundários em cinobactérias, que devem ser levados em consideração ao se estudar estes compostos e suas relações com o ambiente.

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Teplitski, Max I. "Quorum sensing in Sinorhizobium meliloti and effect of plant signals on bacterial quorum sensing." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1029777185.

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Teplitski, Maxim Igorevich. "Quorum sensing in Sinorhizobium meliloti and effect of plant signals on bacterial quorum sensing /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486463803600062.

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Teplitski, Maxim I. "Quorum sensing in Sinorhizobium meliloti and effect of plant signals on bacterial quorum sensing." Columbus, Ohio : Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1029777185.

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Thesis (Ph. D.)--Ohio State University, 2002.<br>Title from first page of PDF file. Document formatted into pages; contains xi, 148 p.; also includes graphics (some col.). Includes abstract and vita. Advisor: Wolfgang D. Bauer, Dept. of Horticulture and Crop Science. Includes bibliographical references (p. 127-148).

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Weber, Marc. "Stochastic Effects in Quorum Sensing." Doctoral thesis, Universitat de Barcelona, 2014. http://hdl.handle.net/10803/276154.

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Stochastic fluctuations, or noise, are ubiquitous in biological systems and play an important role in many cellular processes. Experimental evidences have shown that noise affects the reliability of cell coordination in populations of communicating cells. In this thesis, we study the effects of stochasticity in the emergence of collective behavior in populations of bacteria communicating by QS. We focus on the genetic switch as a paradigm of cellular decision making in both natural and synthetic bacterial systems. Our approach is based on mathematical modeling and stochastic simulations, both at the level of the single cell and at the level of the cell population. We focus on four main topics. In the first topic, we analyze the interplay between intracellular noise and the diffusion process of the QS signaling mechanism. We build a model describing the expression of the signaling molecule and its diffusion in a population of cells, focusing on the situation of very low constitutive expression rate. We show that varying the diffusion rate produces a repertoire of dynamics for the signaling molecule. Our results reveal the contribution of intrinsic noise and transcriptional noise (mRNA copy number fluctuations) in the fluctuations of the signaling molecule. We observe that the total noise exhibits a maximum as a function of the diffusion rate, in contrast to previous studies. Thus, the QS communication mechanism modifies the fluctuations of the signaling molecule inside the cell and interacts with the gene expression noise. In the second topic, we study the effects of gene expression noise on the precision of the population coordination in the QS activation of the LuxR/LuxI system. We analyze the response and dynamics of a population of cells to different levels of autoinducer. Our results show that gene expression noise in LuxR is the main factor that controls the transient variability of the QS activation. This study sheds light on the relation between the single cell stochastic dynamics and the collective behavior in a population of communicating cells. In the third topic, we analyze the effects of intrinsic noise in an autoactivating switch in an isolated single cell. We show that noise promotes the stability of the low-state phenotype of the switch and that the bistable region is extended when increasing the intensity of the fluctuations, an effect that we call stochastic stabilization. Our results show that intrinsic noise modifies the epigenetic landscape as well as the switching rate, which results in complex behavior of the stochastic switching dynamics when varying the intensity of noise. Thus, at the level of a single cell, intrinsic noise contributes to the cell-to-cell variability of the genetic switch and can modify its stable states and its dynamics. In the fourth topic, we build a model of a population of toggle switches communicating by the exchange of two diffusible QS signals. We show that increasing the diffusion rate, which increases the coupling strength between the cells, leads to a phase transition from an unordered phase where the cells randomly flip between the two states of the switch, to an ordered phase with all the cells locked into the same stable state. The same transition is found in a population of cells growing exponentially in a closed volume. Moreover, the response of the cells to a varying external signal exhibits a hysteresis loop. We show that the cell-cell coupling enhances the sensitivity of the population response to the external signal and suggest that this new mechanism could be used to increase the robustness and sensitivity of biosensors. Our results suggest a new mechanism for collective cell decision making based on the phenomenon of phase transition.<br>En aquesta tesi, estudiem els efectes de la estocàsticitat en la aparició del comportament col·lectiu en poblacions de bacteris que comuniquen per quorum sensing (QS). Ens centrem en el interruptor genètic com a paradigma dels processos de decisió cel·lulars tant en sistemes de bacteris naturals com sintètics. El nostre mètode es basa en la modelització matemàtica i en les simulacions estocàstiques, tant a nivell d'una cèl·lula individual com a nivell d'una població de cèl·lules. A nivell d'una cèl·lula individual, mostrem que el soroll afavoreix l'estabilitat del fenotip de l'estat ``baix'' de l'interruptor genètic autoactivador i que la regió de biestabilitat s'estén quan creix la intensitat de les fluctuacions, un efecte que hem anomenat estabilització estocàstica. A nivell d'una població de cèl·lules, mostrem que el procés de difusió del mecanisme de QS modifica les fluctuacions i la dinàmica de la molècula autoinductora dins de la cèl·lula i interactua amb el soroll en la expressió genètica. En el sistema canònic de QS LuxR/LuxI, mostrem que el soroll en la expressió genètica de LuxR és el principal factor que controla la variabilitat transitòria de l'activació del QS. El soroll intrínsec disminueix la precisió de la coordinació de la població i modifica la dinàmica de la transició de QS. A més, presentem un model d'una població d'interruptors genètics de toggle switch que comuniquen per l'intercanvi de dos senyals difusius de QS. Mostrem que l'increment de la velocitat de difusió, que augmenta la força de l'acoblament entre les cèl·lules, porta a una transició de fase: va des d'una fase desordenada on les cèl·lules salten de manera aleatòria entre els dos estats de l'interruptor, fins a una fase ordenada amb totes les cèl·lules bloquejades en el mateix estat estable. La mateixa transició s'ha trobat en una població de cèl·lules que creixen exponencialment en un volum tancat, amb totes les cèl·lules entrant en l'estat ordenat quan arriben a una mida crítica del sistema. Els nostres resultats suggereixen un nou mecanisme per la decisió cel·lular col·lectiva basat en el fenomen de la transició de fase.

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Lewenza, William Shawn. "Quorum sensing in Burkholderia cepacia." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0017/NQ54796.pdf.

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Isherwood, Karen Elizabeth. "Quorum sensing in Yersinia pestis." Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364667.

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Atkinson, Steven. "Quorum sensing in Yersinia pseudotuberculosis." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287185.

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Hardman, Andrea M. "Quorum sensing in vibrio anguillarum." Thesis, University of Nottingham, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363936.

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Buckley, Catherine M. F. "Quorum sensing in Yersinia pseudotuberculosis." Thesis, University of Nottingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273108.

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Libri sul tema "Quorum sensing"

Rumbaugh, Kendra P., ed. Quorum Sensing. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-971-0.

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Leoni, Livia, and Giordano Rampioni, eds. Quorum Sensing. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7309-5.

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Kalia, Vipin Chandra, ed. Biotechnological Applications of Quorum Sensing Inhibitors. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-9026-4.

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Kalia, Vipin Chandra, ed. Quorum Sensing and its Biotechnological Applications. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-0848-2.

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Dhiman, Saurabh Sudha, ed. Quorum Sensing: Microbial Rules of Life. Washington, DC: American Chemical Society, 2020. http://dx.doi.org/10.1021/bk-2020-1374.

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Kalia, Vipin Chandra, ed. Quorum Sensing vs Quorum Quenching: A Battle with No End in Sight. New Delhi: Springer India, 2015. http://dx.doi.org/10.1007/978-81-322-1982-8.

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Mattias, Collin, and Schuch Raymond, eds. Bacterial sensing and signaling. Basel : New York: Karger, 2009.

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Pallaval Veera Bramhachari, ed. Implication of Quorum Sensing System in Biofilm Formation and Virulence. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-2429-1.

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Sebaihia, Mohammed. Quorum sensing and carbapenem antibiotic production in Erwinia carotovora subspecies carotovora. [s.l.]: typescript, 1999.

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Bramhachari, Pallaval Veera, ed. Implication of Quorum Sensing and Biofilm Formation in Medicine, Agriculture and Food Industry. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9409-7.

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Capitoli di libri sul tema "Quorum sensing"

Amils, Ricardo. "Quorum Sensing." In Encyclopedia of Astrobiology, 1397. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-11274-4_1328.

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Bassler, Bonnie L., and Melissa B. Miller. "Quorum Sensing." In The Prokaryotes, 495–509. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-30123-0_60.

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Amils, Ricardo. "Quorum Sensing." In Encyclopedia of Astrobiology, 2104. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-44185-5_1328.

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Medina-Martínez, María S., and María Angélica Santana. "Quorum Sensing." In Decontamination of Fresh and Minimally Processed Produce, 333–44. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118229187.ch19.

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Bassler, Bonnie L., and Melissa B. Miller. "Quorum Sensing." In The Prokaryotes, 336–53. New York, NY: Springer New York, 2006. http://dx.doi.org/10.1007/0-387-30742-7_12.

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Amils, Ricardo. "Quorum Sensing." In Encyclopedia of Astrobiology, 2556. Berlin, Heidelberg: Springer Berlin Heidelberg, 2023. http://dx.doi.org/10.1007/978-3-662-65093-6_1328.

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Pesci, Everett C., and Barbara H. Iglewski. "Quorum Sensing." In Bacterial Protein Toxins, 55–65. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817893.ch4.

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Bhunia, Archisman, Kumar Narayan, Abhilasha Singh, Asmeeta Sircar, and Nivedita Chatterjee. "Quorum Sensing." In Omics for Environmental Engineering and Microbiology Systems, 85–111. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003247883-5.

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Nag, Moupriya, Dibyajit Lahiri, Anushka Ghosh, Deboleena Das, and Rina Rani Ray. "Quorum Sensing." In Biofilm-Mediated Diseases: Causes and Controls, 21–45. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-0745-5_2.

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Swift, Simon, Maria C. Rowe, and Malavika Kamath. "Quorum Sensing." In Bacterial Physiology, 179–232. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-74921-9_7.

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Atti di convegni sul tema "Quorum sensing"

Beckmann, Benjamin E., and Philip K. McKinley. "Evolving quorum sensing in digital organisms." In the 11th Annual conference. New York, New York, USA: ACM Press, 2009. http://dx.doi.org/10.1145/1569901.1569916.

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Vogt, Ryan, John Aycock, and Michael J. Jacobson. "Quorum sensing and self-stopping worms." In the 2007 ACM workshop. New York, New York, USA: ACM Press, 2007. http://dx.doi.org/10.1145/1314389.1314394.

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Peysakhov, Maxim, Christopher Dugan, Pragnesh Jay Modi, and William Regli. "Quorum sensing on mobile ad-hoc networks." In the fifth international joint conference. New York, New York, USA: ACM Press, 2006. http://dx.doi.org/10.1145/1160633.1160831.

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Michelusi, Nicolo. "On population density estimation via quorum sensing." In 2017 15th Canadian Workshop on Information Theory (CWIT). IEEE, 2017. http://dx.doi.org/10.1109/cwit.2017.7994827.

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Abadal, Sergi, Ignacio Llatser, Eduard Alarcon, and Albert Cabellos-Aparicio. "Quorum Sensing-enabled amplification for molecular nanonetworks." In ICC 2012 - 2012 IEEE International Conference on Communications. IEEE, 2012. http://dx.doi.org/10.1109/icc.2012.6364691.

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Beckmann, Benjamin E., Philip K. McKinley, and David B. Knoester. "Effects of Communication Impairments on Quorum Sensing." In 2009 Third IEEE International Conference on Self-Adaptive and Self-Organizing Systems (SASO). IEEE, 2009. http://dx.doi.org/10.1109/saso.2009.37.

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O’Sullivan, Timothy P. "Small Molecule Inhibitors of Bacterial Quorum Sensing." In ECMC 2022. Basel Switzerland: MDPI, 2022. http://dx.doi.org/10.3390/ecmc2022-13264.

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Vasconcelos, Marcos M., Urbashi Mitra, Odilon Camara, Kalinga Pavan Silva, and James Boedicker. "Bacterial Quorum Sensing as a Networked Decision System." In 2018 IEEE International Conference on Communications (ICC 2018). IEEE, 2018. http://dx.doi.org/10.1109/icc.2018.8422668.

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Cho, Jae Hoon, Jin il Park, Ji Seok Jeong, and Myung Geun Chun. "Bacterial foraging with quorum sensing based optimization algorithm." In 2009 IEEE International Conference on Fuzzy Systems (FUZZ-IEEE). IEEE, 2009. http://dx.doi.org/10.1109/fuzzy.2009.5277169.

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Barani, Navid, and Kamal Sarabandi. "Biological Cell Communication: Quorum Sensing Versus Electromagnetic Signaling." In 2020 IEEE USNC-CNC-URSI North American Radio Science Meeting (Joint with AP-S Symposium). IEEE, 2020. http://dx.doi.org/10.23919/usnc/ursi49741.2020.9321612.

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Rapporti di organizzazioni sul tema "Quorum sensing"

Library, Spring. Where Does Current Quorum Sensing Research Stand. Spring Library, December 2020. http://dx.doi.org/10.47496/sl.blog.16.

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Abstract (sommario):

Quorum quenching is achieved by inactivating signalling enzymes, by introducing molecules that mimic signalling molecules and block their receptors, by degrading signalling molecules themselves, or by a modification of the quorum sensing signals due to an enzyme activity.

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Rinker-Schaeffer, Carrie. Societal Interactions in Ovarian Cancer Metastases: Quorum-Sensing Hypothesis. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada481442.

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Ognibene, Ted J., N. Young, A. Holtz-Morris, and P. Daley. Identification of Pathways Critical to Quorum Sensing and Virulence Induction. Office of Scientific and Technical Information (OSTI), February 2009. http://dx.doi.org/10.2172/1114715.

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Segelke, B., S. Hok, V. Lao, M. Corzett, and E. Garcia. Regulation of Yersina pestis Virulence by AI-2 Mediated Quorum Sensing. Office of Scientific and Technical Information (OSTI), March 2010. http://dx.doi.org/10.2172/978400.

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Ulrich, Ricky L., David DeShazer, Harry B. Hines, and Jeffrey A. Jeddeloh. Quorum Sensing: A transcriptional Regulatory System Involved in the Pathogenicity of Burkholderia mallei. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada429432.

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Helman, Yael, Mikael Elias, and Al Aksan. potential use of a highly-stable lactonase from hyperthermophilic archaea for disruption of quorum sensing in soft rot Pectobacteria. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604284.bard.

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Splitter, Gary, and Menachem Banai. Microarray Analysis of Brucella melitensis Pathogenesis. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7709884.bard.

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Original Objectives 1. To determine the Brucella genes that lead to chronic macrophage infection. 2. To identify Brucella genes that contribute to infection. 3. To confirm the importance of Brucella genes in macrophages and placental cells by mutational analysis. Background Brucella spp. is a Gram-negative facultative intracellular bacterium that infects ruminants causing abortion or birth of severely debilitated animals. Brucellosis continues in Israel, caused by B. melitensis despite an intensive eradication campaign. Problems with the Rev1 vaccine emphasize the need for a greater understanding of Brucella pathogenesis that could improve vaccine designs. Virulent Brucella has developed a successful strategy for survival in its host and transmission to other hosts. To invade the host, virulent Brucella establishes an intracellular niche within macrophages avoiding macrophage killing, ensuring its long-term survival. Then, to exit the host, Brucella uses placenta where it replicates to high numbers resulting in abortion. Also, Brucella traffics to the mammary gland where it is secreted in milk. Missing from our understanding of brucellosis is the surprisingly lillie basic information detailing the mechanisms that permit bacterial persistence in infected macrophages (chronic infection) and dissemination to other animals from infected placental cells and milk (acute infection). Microarray analysis is a powerful approach to determine global gene expression in bacteria. The close genomic similarities of Brucella species and our recent comparative genomic studies of Brucella species using our B. melitensis microarray, suqqests that the data obtained from studying B. melitensis 16M would enable understanding the pathogenicity of other Brucella organisms, particularly the diverse B. melitensis variants that confound Brucella eradication in Israel. Conclusions Results from our BARD studies have identified previously unknown mechanisms of Brucella melitensis pathogenesis- i.e., response to blue light, quorum sensing, second messenger signaling by cyclic di-GMP, the importance of genomic island 2 for lipopolysaccharide in the outer bacterial membrane, and the role of a TIR domain containing protein that mimics a host intracellular signaling molecule. Each one of these pathogenic mechanisms offers major steps in our understanding of Brucella pathogenesis. Strikingly, our molecular results have correlated well to the pathognomonic profile of the disease. We have shown that infected cattle do not elicit antibodies to the organisms at the onset of infection, in correlation to the stealth pathogenesis shown by a molecular approach. Moreover, our field studies have shown that Brucella exploit this time frame to transmit in nature by synchronizing their life cycle to the gestation cycle of their host succumbing to abortion in the last trimester of pregnancy that spreads massive numbers of organisms in the environment. Knowing the bacterial mechanisms that contribute to the virulence of Brucella in its host has initiated the agricultural opportunities for developing new vaccines and diagnostic assays as well as improving control and eradication campaigns based on herd management and linking diagnosis to the pregnancy status of the animals. Scientific and Agricultural Implications Our BARD funded studies have revealed important Brucella virulence mechanisms of pathogenesis. Our publication in Science has identified a highly novel concept where Brucella utilizes blue light to increase its virulence similar to some plant bacterial pathogens. Further, our studies have revealed bacterial second messengers that regulate virulence, quorum sensing mechanisms permitting bacteria to evaluate their environment, and a genomic island that controls synthesis of its lipopolysaccharide surface. Discussions are ongoing with a vaccine company for application of this genomic island knowledge in a Brucella vaccine by the U.S. lab. Also, our new technology of bioengineering bioluminescent Brucella has resulted in a spin-off application for diagnosis of Brucella infected animals by the Israeli lab by prioritizing bacterial diagnosis over serological diagnosis.

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Coplin, David L., Shulamit Manulis, and Isaac Barash. roles Hrp-dependent effector proteins and hrp gene regulation as determinants of virulence and host-specificity in Erwinia stewartii and E. herbicola pvs. gypsophilae and betae. United States Department of Agriculture, June 2005. http://dx.doi.org/10.32747/2005.7587216.bard.

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Gram-negative plant pathogenic bacteria employ specialized type-III secretion systems (TTSS) to deliver an arsenal of pathogenicity proteins directly into host cells. These secretion systems are encoded by hrp genes (for hypersensitive response and pathogenicity) and the effector proteins by so-called dsp or avr genes. The functions of effectors are to enable bacterial multiplication by damaging host cells and/or by blocking host defenses. We characterized essential hrp gene clusters in the Stewart's Wilt of maize pathogen, Pantoea stewartii subsp. stewartii (Pnss; formerly Erwinia stewartii) and the gall-forming bacterium, Pantoea agglomerans (formerly Erwinia herbicola) pvs. gypsophilae (Pag) and betae (Pab). We proposed that the virulence and host specificity of these pathogens is a function of a) the perception of specific host signals resulting in bacterial hrp gene expression and b) the action of specialized signal proteins (i.e. Hrp effectors) delivered into the plant cell. The specific objectives of the proposal were: 1) How is the expression of the hrp and effector genes regulated in response to host cell contact and the apoplastic environment? 2) What additional effector proteins are involved in pathogenicity? 3) Do the presently known Pantoea effector proteins enter host cells? 4) What host proteins interact with these effectors? We characterized the components of the hrp regulatory cascade (HrpXY ->7 HrpS ->7 HrpL ->7 hrp promoters), showed that they are conserved in both Pnss and Fag, and discovered that the regulation of the hrpS promoter (hrpSp) may be a key point in integrating apoplastic signals. We also analyzed the promoters recognized by HrpL and demonstrated the relationship between their composition and efficiency. Moreover, we showed that promoter strength can influence disease expression. In Pnss, we found that the HrpXY two-component signal system may sense the metabolic status of the bacterium and is required for full hrp gene expression in planta. In both species, acyl-homoserine lactone-mediated quorum sensing may also regulate epiphytic fitness and/or pathogenicity. A common Hrp effector protein, DspE/WtsE, is conserved and required for virulence of both species. When introduced into corn cells, Pnss WtsE protein caused water-soaked lesions. In other plants, it either caused cell death or acted as an Avr determinant. Using a yeast- two-hybrid system, WtsE was shown to interact with a number of maize signal transduction proteins that are likely to have roles in either programmed cell death or disease resistance. In Pag and Pab, we have characterized the effector proteins HsvG, HsvB and PthG. HsvG and HsvB are homologous proteins that determine host specificity of Pag and Pab on gypsophila and beet, respectively. Both possess a transcriptional activation domain that functions in yeast. PthG was found to act as an Avr determinant on multiple beet species, but was required for virulence on gypsophila. In addition, we demonstrated that PthG acts within the host cell. Additional effector genes have been characterized on the pathogenicity plasmid, pPATHₚₐg, in Pag. A screen for HrpL- regulated genes in Pnsspointed up 18 candidate effector proteins and four of these were required for full virulence. It is now well established that the virulence of Gram-negative plant pathogenic bacteria is governed by Hrp-dependent effector proteins. However; the mode of action of many effectors is still unresolved. This BARD supported research will significantly contribute to the understanding of how Hrp effectors operate in Pantoea spp. and how they control host specificity and affect symptom production. This may lead to novel approaches for genetically engineering plants resistant to a wide range of bacterial pathogens by inactivating the Hrp effectors with "plantabodies" or modifying their receptors, thereby blocking the induction of the susceptible response. Alternatively, innovative technologies could be used to interfere with the Hrp regulatory cascade by blocking a critical step or mimicking plant or quorum sensing signals.

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Yedidia, I., H. Senderowitz, and A. O. Charkowski. Small molecule cocktails designed to impair virulence targets in soft rot Erwinias. Israel: United States-Israel Binational Agricultural Research and Development Fund, 2020. http://dx.doi.org/10.32747/2020.8134165.bard.

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Chemical signaling between beneficial or pathogenic bacteria and plants is a central factor in determining the outcome of plant-microbe interactions. Pectobacterium and Dickeya (soft rot Erwinias) are the major cause of soft rot, stem rot, and blackleg formed on potato and ornamentals, currently with no effective control. Our major aim was to establish and study specific bacterial genes/proteins as targets for anti-virulence compounds, by combining drug design tools and bioinformatics with experimental work. The approach allowed us to identify and test compounds (small molecules) that specifically interfere with the activities of these targets, by this impairing bacterial virulence. Two main targets were selected within the frame of the BARD project. The first is the ATP-binding cassette (ABC) transporters and methyl-accepting chemotaxis proteins (MCP) that have been characterized here for the first time in Pectobacteriaceae, and the second is the quorum sensing (QS) machinery of Pectobacterium with its major proteins and in particular, the AHL synthase ExpI that was identified as the preferred target for inhibition. Both systems are strongly associated with bacterial virulence and survival in planta. We found that Pectobacteriaceae, namely Dickeya and Pectobacterium, encode more ABC transporters and MCP in their genomes, compared to other bacteria in the order. For MCP, soft rot Pectobacteriaceae not only contain more than 30 MCP genes per strain, but also have more diverse ligand binding domains than other species in the Enterobacteriales. These findings suggest that both ABC transporters and MCP are important for soft rot Pectobacteriaceae pathogenicity. We now have a selection of mutants in these proteins that may be further explored to understand their direct involvement in virulence. In parallel, we studied the QS central proteins in pectobacteria, the signaling molecule N-acyl-homoserine lactone synthase, ExpI, and the response regulator ExpR, and established their phylogenetic relations within plant pathogenic Gram negative bacteria. Next, these proteins were used for virtual screening of millions of compounds in order to discover new compounds with potential to interfere with the QS machinery. Several natural compounds were tested for their interference with virulence related traits in Pectobacterium and their capability to minimize soft rot infections. Our findings using microcalorimetric binding studies have established for the first time direct interaction between the protein ExpI and two natural ligands, the plant hormone salicylic acid and the volatile compound carvacrol. These results supported a model by which plants interfere with bacterial communication through interkingdom signaling. The collaborative project yielded two research papers and a comprehensive review, which included new computational and bioinformatics data, in Annu. Rev. Phytopathol., the highest ranked journal in phytopathology. Additional two papers are in preparation. In order to transform the fundamental knowledge that have been gained during this collaborative BARD project into agricultural practice, to control soft rot bacteria, we have submitted a continual project.

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Ron, Eliora, and Eugene Eugene Nester. Global functional genomics of plant cell transformation by agrobacterium. United States Department of Agriculture, March 2009. http://dx.doi.org/10.32747/2009.7695860.bard.

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The aim of this study was to carry out a global functional genomics analysis of plant cell transformation by Agrobacterium in order to define and characterize the physiology of Agrobacterium in the acidic environment of a wounded plant. We planed to study the proteome and transcriptome of Agrobacterium in response to a change in pH, from 7.2 to 5.5 and identify genes and circuits directly involved in this change. Bacteria-plant interactions involve a large number of global regulatory systems, which are essential for protection against new stressful conditions. The interaction of bacteria with their hosts has been previously studied by genetic-physiological methods. We wanted to make use of the new capabilities to study these interactions on a global scale, using transcription analysis (transcriptomics, microarrays) and proteomics (2D gel electrophoresis and mass spectrometry). The results provided extensive data on the functional genomics under conditions that partially mimic plant infection and – in addition - revealed some surprising and significant data. Thus, we identified the genes whose expression is modulated when Agrobacterium is grown under the acidic conditions found in the rhizosphere (pH 5.5), an essential environmental factor in Agrobacterium – plant interactions essential for induction of the virulence program by plant signal molecules. Among the 45 genes whose expression was significantly elevated, of special interest is the two-component chromosomally encoded system, ChvG/I which is involved in regulating acid inducible genes. A second exciting system under acid and ChvG/Icontrol is a secretion system for proteins, T6SS, encoded by 14 genes which appears to be important for Rhizobium leguminosarum nodule formation and nitrogen fixation and for virulence of Agrobacterium. The proteome analysis revealed that gamma aminobutyric acid (GABA), a metabolite secreted by wounded plants, induces the synthesis of an Agrobacterium lactonase which degrades the quorum sensing signal, N-acyl homoserine lactone (AHL), resulting in attenuation of virulence. In addition, through a transcriptomic analysis of Agrobacterium growing at the pH of the rhizosphere (pH=5.5), we demonstrated that salicylic acid (SA) a well-studied plant signal molecule important in plant defense, attenuates Agrobacterium virulence in two distinct ways - by down regulating the synthesis of the virulence (vir) genes required for the processing and transfer of the T-DNA and by inducing the same lactonase, which in turn degrades the AHL. Thus, GABA and SA with different molecular structures, induce the expression of these same genes. The identification of genes whose expression is modulated by conditions that mimic plant infection, as well as the identification of regulatory molecules that help control the early stages of infection, advance our understanding of this complex bacterial-plant interaction and has immediate potential applications to modify it. We expect that the data generated by our research will be used to develop novel strategies for the control of crown gall disease. Moreover, these results will also provide the basis for future biotechnological approaches that will use genetic manipulations to improve bacterial-plant interactions, leading to more efficient DNA transfer to recalcitrant plants and robust symbiosis. These advances will, in turn, contribute to plant protection by introducing genes for resistance against other bacteria, pests and environmental stress.

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