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dc.contributor.authorRasheedkhan Regina, Viduthalaien_US
dc.contributor.authorNoorian, Parisaen_US
dc.contributor.authorSim, Clarence Bo Wenen_US
dc.contributor.authorConstancias, Florentinen_US
dc.contributor.authorKaliyamoorthy, Eganathanen_US
dc.contributor.authorBooth, Sean C.en_US
dc.contributor.authorEspinoza-Vergara, Gustavoen_US
dc.contributor.authorRice, Scott A.en_US
dc.contributor.authorMcDougald, Dianeen_US
dc.identifier.citationRasheedkhan Regina, V., Noorian, P., Sim, C. B. W., Constancias, F., Kaliyamoorthy, E., Booth, S. C., Espinoza-Vergara, G., Rice, S. A. & McDougald, D. (2022). Loss of the acetate switch in Vibrio vulnificus enhances predation defense against Tetrahymena pyriformis. Applied and Environmental Microbiology, 88(2), e01665-21-.
dc.description.abstractVibrio vulnificus is an opportunistic human pathogen and autochthonous inhabitant of coastal marine environments, where the bacterium is under constant predation by heterotrophic protists or protozoans. As a result of this selection pressure, genetic variants with antipredation mechanisms are selected for and persist in the environment. Such natural variants may also be pathogenic to animal or human hosts, making it important to understand these defense mechanisms. To identify antipredator strategies, 13 V. vulnificus strains of different genotypes isolated from diverse environments were exposed to predation by the ciliated protozoan Tetrahymena pyriformis, and only strain ENV1 was resistant to predation. Further investigation of the cell-free supernatant showed that ENV1 acidifies the environment by the excretion of organic acids, which are toxic to T. pyriformis. As this predation resistance was dependent on the availability of iron, transcriptomes of V. vulnificus in iron-replete and iron-deplete conditions were compared. This analysis revealed that ENV1 ferments pyruvate and the resultant acetyl-CoA leads to acetate synthesis under aerobic conditions, a hallmark of overflow metabolism. The anaerobic respiration global regulator arcA was upregulated when iron was available. An ΔarcA deletion mutant of ENV1 accumulated less acetate and, importantly, was sensitive to grazing by T. pyriformis. Based on the transcriptome response and quantification of metabolites, we conclude that ENV1 has adapted to overflow metabolism and has lost a control switch that shifts metabolism from acetate excretion to acetate assimilation, enabling it to excrete acetate continuously. We show that overflow metabolism and the acetate switch contribute to prey-predator interactions. IMPORTANCE Bacteria in the environment, including Vibrio spp., interact with protozoan predators. To defend against predation, bacteria evolve antipredator mechanisms ranging from changing morphology, biofilm formation, and secretion of toxins or virulence factors. Some of these adaptations may result in strains that are pathogenic to humans. Therefore, it is important to study predator defense strategies of environmental bacteria. V. vulnificus thrives in coastal waters and infects humans. Very little is known about the defense mechanisms V. vulnificus expresses against predation. Here, we show that a V. vulnificus strain (ENV1) has rewired the central carbon metabolism, enabling the production of excess organic acid that is toxic to the protozoan predator T. pyriformis. This is a previously unknown mechanism of predation defense that protects against protozoan predators.en_US
dc.description.sponsorshipMinistry of Education (MOE)en_US
dc.description.sponsorshipNational Research Foundation (NRF)en_US
dc.relation.ispartofApplied and Environmental Microbiologyen_US
dc.rights© 2022 Rasheedkhan Regina et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.en_US
dc.subjectScience::Biological sciencesen_US
dc.titleLoss of the acetate switch in Vibrio vulnificus enhances predation defense against Tetrahymena pyriformisen_US
dc.typeJournal Articleen
dc.contributor.schoolSchool of Biological Sciencesen_US
dc.contributor.researchSingapore Centre for Environmental Life Sciences and Engineering (SCELSE)en_US
dc.description.versionPublished versionen_US
dc.subject.keywordsProtozoan Predationen_US
dc.subject.keywordsGrazing Resistanceen_US
dc.description.acknowledgementWe acknowledge support from the iThree Institute at the University of Technology Sydney, Sydney, Australia, the Australian Research Council Discovery Project (DP170100453) and by the National Research Foundation and Ministry of Education Singapore under its Research Centre of Excellence Program to the Singapore Centre for Environmental Life Sciences Engineering, Nanyang Technological University.en_US
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