scholarly journals Ferric Uptake Regulator Fur Coordinates Siderophore Production and Defense against Iron Toxicity and Oxidative Stress and Contributes to Virulence in Chromobacterium violaceum

2020 ◽  
Vol 86 (21) ◽  
Author(s):  
Renato Elias Rodrigues de Souza Santos ◽  
Bianca Bontempi Batista ◽  
José Freire da Silva Neto
Keyword(s):  
Oxidative Stress ◽  
Biofilm Formation ◽  
Chromobacterium Violaceum ◽  
Siderophore Production ◽  
Phenotypic Characterization ◽  
Ferric Uptake Regulator ◽  
Content Type ◽  
Swimming Motility ◽  
Oxidative Stresses ◽  
Major Player

ABSTRACT Iron is a highly reactive metal that participates in several processes in prokaryotic and eukaryotic cells. Hosts and pathogens compete for iron in the context of infection. Chromobacterium violaceum, an environmental Gram-negative bacterial pathogen, relies on siderophores to overcome iron limitation in the host. In this work, we studied the role of the ferric uptake regulator Fur in the physiology and virulence of C. violaceum. A Δfur mutant strain showed decreased growth and fitness under regular in vitro growth conditions and presented high sensitivity to iron and oxidative stresses. Furthermore, the absence of fur caused derepression of siderophore production and reduction in swimming motility and biofilm formation. Consistent with these results, the C. violaceum Δfur mutant was highly attenuated for virulence and liver colonization in mice. In contrast, a manganese-selected spontaneous fur mutant showed only siderophore overproduction and sensitivity to oxidative stress, indicating that Fur remained partially functional in this strain. We found that mutations in genes related to siderophore biosynthesis and a putative CRISPR-Cas locus rescued the Δfur mutant growth defects, indicating that multiple Fur-regulated processes contribute to maintaining bacterial cell fitness. Overall, our data indicated that Fur is conditionally essential in C. violaceum mainly by protecting cells from iron overload and oxidative damage. The requirement of Fur for virulence highlights the importance of iron in the pathogenesis of C. violaceum. IMPORTANCE Maintenance of iron homeostasis, i.e., avoiding both deficiency and toxicity of this metal, is vital to bacteria and their hosts. Iron sequestration by host proteins is a crucial strategy to combat bacterial infections. In bacteria, the ferric uptake regulator Fur coordinates the expression of several iron-related genes. Sometimes, Fur can also regulate several other processes. In this work, we performed an in-depth phenotypic characterization of fur mutants in the human opportunistic pathogen Chromobacterium violaceum. We determined that fur is a conditionally essential gene necessary for proper growth under regular conditions and is fully required for survival under iron and oxidative stresses. Fur also controlled several virulence-associated traits, such as swimming motility, biofilm formation, and siderophore production. Consistent with these results, a C. violaceum fur null mutant showed attenuation of virulence. Therefore, our data established Fur as a major player required for C. violaceum to manage iron, including during infection in the host.

scholarly journals Ferric Uptake Regulator (FurA) is Required for Acidovorax citrulli Virulence on Watermelon

2019 ◽  
Vol 109 (12) ◽  
pp. 1997-2008 ◽  
Author(s):  
Jun Liu ◽  
Yanli Tian ◽  
Yuqiang Zhao ◽  
Rong Zeng ◽  
Baohui Chen ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Biofilm Formation ◽  
Crop Production ◽  
Deletion Mutant ◽  
Manganese Superoxide Dismutase ◽  
Siderophore Production ◽  
Ferric Uptake Regulator ◽  
Swimming Motility ◽  
Acidovorax Citrulli

Acidovorax citrulli is the causal agent of bacterial fruit blotch, a serious threat to commercial watermelon and melon crop production worldwide. Ferric uptake regulator (Fur) is a global transcription factor that affects a number of virulence-related functions in phytopathogenic bacteria; however, the role of furA has not been determined for A. citrulli. Hence, we constructed an furA deletion mutant and a corresponding complement in the background of A. citrulli strain xlj12 to investigate the role of the gene in siderophore production, concentration of intracellular Fe2+, bacterial sensitivity to hydrogen peroxide, biofilm formation, swimming motility, hypersensitive response induction, and virulence on melon seedlings. The A. citrulli furA deletion mutant displayed increased siderophore production, intracellular Fe2+ concentration, and increased sensitivity to hydrogen peroxide. In contrast, biofilm formation, swimming motility, and virulence on melon seedlings were significantly reduced in the furA mutant. As expected, complementation of the furA deletion mutant restored all phenotypes to wild-type levels. In accordance with the phenotypic results, the expression levels of bfrA and bfrB that encode bacterioferritin, sodB that encodes iron/manganese superoxide dismutase, fliS that encodes a flagellar protein, hrcN that encodes the type III secretion system (T3SS) ATPase, and hrcC that encodes the T3SS outer membrane ring protein were significantly downregulated in the A. citrulli furA deletion mutant. In addition, the expression of feo-related genes and feoA and feoB was significantly upregulated in the furA mutant. Overall, these results indicated that, in A. citrulli, FurA contributes to the regulation of the iron balance system, and affects a variety of virulence-related traits.

scholarly journals Identification of FDA-Approved Drugs as Antivirulence Agents Targeting the pqs Quorum-Sensing System of Pseudomonas aeruginosa

2018 ◽  
Vol 62 (11) ◽  
Author(s):  
Francesca D'Angelo ◽  
Valerio Baldelli ◽  
Nigel Halliday ◽  
Paolo Pantalone ◽  
Fabio Polticelli ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Biofilm Formation ◽  
Antifungal Drugs ◽  
Phenotypic Characterization ◽  
Resistant Bacteria ◽  
Gram Positive ◽  
Active Inhibitor ◽  
Content Type ◽  
Approved Drugs

ABSTRACT The long-term use of antibiotics has led to the emergence of multidrug-resistant bacteria. A promising strategy to combat bacterial infections aims at hampering their adaptability to the host environment without affecting growth. In this context, the intercellular communication system quorum sensing (QS), which controls virulence factor production and biofilm formation in diverse human pathogens, is considered an ideal target. Here, we describe the identification of new inhibitors of the pqs QS system of the human pathogen Pseudomonas aeruginosa by screening a library of 1,600 U.S. Food and Drug Administration-approved drugs. Phenotypic characterization of ad hoc engineered strains and in silico molecular docking demonstrated that the antifungal drugs clotrimazole and miconazole, as well as an antibacterial compound active against Gram-positive pathogens, clofoctol, inhibit the pqs system, probably by targeting the transcriptional regulator PqsR. The most active inhibitor, clofoctol, specifically inhibited the expression of pqs-controlled virulence traits in P. aeruginosa, such as pyocyanin production, swarming motility, biofilm formation, and expression of genes involved in siderophore production. Moreover, clofoctol protected Galleria mellonella larvae from P. aeruginosa infection and inhibited the pqs QS system in P. aeruginosa isolates from cystic fibrosis patients. Notably, clofoctol is already approved for clinical treatment of pulmonary infections caused by Gram-positive bacterial pathogens; hence, this drug has considerable clinical potential as an antivirulence agent for the treatment of P. aeruginosa lung infections.

scholarly journals Tryptophan Inhibits Biofilm Formation by Pseudomonas aeruginosa

2013 ◽  
Vol 57 (4) ◽  
pp. 1921-1925 ◽  
Author(s):  
Kenneth S. Brandenburg ◽  
Karien J. Rodriguez ◽  
Jonathan F. McAnulty ◽  
Christopher J. Murphy ◽  
Nicholas L. Abbott ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Tissue Culture ◽  
Biofilm Formation ◽  
Chronic Wounds ◽  
Inhibitory Effect ◽  
Equimolar Ratio ◽  
Biofilm Growth ◽  
Content Type ◽  
Swimming Motility

ABSTRACTBiofilm formation byPseudomonas aeruginosahas been implicated in the pathology of chronic wounds. Both thedandlisoforms of tryptophan inhibitedP. aeruginosabiofilm formation on tissue culture plates, with an equimolar ratio ofdandlisoforms producing the greatest inhibitory effect. Addition ofd-/l-tryptophan to existing biofilms inhibited further biofilm growth and caused partial biofilm disassembly. Tryptophan significantly increased swimming motility, which may be responsible in part for diminished biofilm formation byP. aeruginosa.

scholarly journals The Cch1-Mid1 High-Affinity Calcium Channel Contributes to the Virulence of Cryptococcus neoformans by Mitigating Oxidative Stress

2015 ◽  
Vol 14 (11) ◽  
pp. 1135-1143 ◽  
Author(s):  
Kiem Vu ◽  
Jennifer M. Bautos ◽  
Angie Gelli
Keyword(s):  
Oxidative Stress ◽  
Cryptococcus Neoformans ◽  
Defense Mechanisms ◽  
Pathogenic Fungi ◽  
Growth Defect ◽  
Compensatory Mechanism ◽  
General Role ◽  
Content Type ◽  
High Affinity ◽  
Oxidative Stresses

ABSTRACT Pathogenic fungi have developed mechanisms to cope with stresses imposed by hosts. For Cryptococcus spp., this implies active defense mechanisms that attenuate and ultimately overcome the onslaught of oxidative stresses in macrophages. Among cellular pathways within Cryptococcus neoformans ' arsenal is the plasma membrane high-affinity Cch1-Mid1 calcium (Ca 2+ ) channel (CMC). Here we show that CMC has an unexpectedly complex and disparate role in mitigating oxidative stress. Upon inhibiting the Ccp1-mediated oxidative response pathway with antimycin, strains of C. neoformans expressing only Mid1 displayed enhanced growth, but this was significantly attenuated upon H 2 O 2 exposure in the absence of Mid1, suggesting a regulatory role for Mid1 acting through the Ccp1-mediated oxidative stress response. This notion is further supported by the interaction detected between Mid1 and Ccp1 (cytochrome c peroxidase). In contrast, Cch1 appears to have a more general role in promoting cryptococci survival during oxidative stress. A strain lacking Cch1 displayed a growth defect in the presence of H 2 O 2 without BAPTA [(1,2-bis(2-aminophenoxy)ethane- N , N , N ′, N ′-tetraacetic acid, cesium salt] or additional stressors such as antimycin. Consistent with a greater contribution of Cch1 to oxidative stress tolerance, an intracellular growth defect was observed for the cch1 Δ strain in the macrophage cell line J774A.1. Interestingly, while the absence of either Mid1 or Cch1 significantly compromises the ability of C. neoformans to tolerate oxidative stress, the absence of both Mid1 and Cch1 has a negligible effect on C. neoformans growth during H 2 O 2 stress, suggesting the existence of a compensatory mechanism that becomes active in the absence of CMC.

scholarly journals Deletion Mutant Library for Investigation of Functional Outputs of Cyclic Diguanylate Metabolism in Pseudomonas aeruginosa PA14

2014 ◽  
Vol 80 (11) ◽  
pp. 3384-3393 ◽  
Author(s):  
Dae-Gon Ha ◽  
Megan E. Richman ◽  
George A. O'Toole
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Deletion Mutant ◽  
Deletion Mutants ◽  
Mutant Library ◽  
Potential Utility ◽  
Cyclic Diguanylate ◽  
Swarming Motility ◽  
Content Type ◽  
Swimming Motility

ABSTRACTWe constructed a library of in-frame deletion mutants targeting each gene inPseudomonas aeruginosaPA14 predicted to participate in cyclic di-GMP (c-di-GMP) metabolism (biosynthesis or degradation) to provide a toolkit to assist investigators studying c-di-GMP-mediated regulation by this microbe. We present phenotypic assessments of each mutant, including biofilm formation, exopolysaccharide (EPS) production, swimming motility, swarming motility, and twitch motility, as a means to initially characterize these mutants and to demonstrate the potential utility of this library.

scholarly journals Defining Gene-Phenotype Relationships in Acinetobacter baumannii through One-Step Chromosomal Gene Inactivation

mBio ◽  
2014 ◽  
Vol 5 (4) ◽  
Author(s):  
Ashley T. Tucker ◽  
Emily M. Nowicki ◽  
Joseph M. Boll ◽  
Gregory A. Knauf ◽  
Nora C. Burdis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antibiotic Resistance ◽  
Acinetobacter Baumannii ◽  
Genome Editing ◽  
Biofilm Formation ◽  
Content Type ◽  
Stress Protection ◽  
Biocide Resistance ◽  
Hospital Acquired ◽  
Oxidative Stress Protection

ABSTRACTRates of infection with hospital-acquiredAcinetobacter baumanniihave exploded over the past decade due to our inability to limit persistence and effectively treat disease.A. baumanniiquickly acquires antibiotic resistance, and its genome encodes mechanisms to tolerate biocides and desiccation, which enhance its persistence in hospital settings. With depleted antibiotic options, new methods to treatA. baumanniiinfections are desperately needed. A comprehensive understanding detailingA. baumanniicellular factors that contribute to its resiliency at genetic and mechanistic levels is vital to the development of new treatment options. Tools to rapidly dissect theA. baumanniigenome will facilitate this goal by quickly advancing our understanding ofA. baumanniigene-phenotype relationships. We describe here a recombination-mediated genetic engineering (recombineering) system for targeted genome editing ofA. baumannii. We have demonstrated that this system can perform directed mutagenesis on wide-ranging genes and operons and is functional in various strains ofA. baumannii, indicating its broad application. We utilized this system to investigate key gene-phenotype relationships inA. baumanniibiology important to infection and persistence in hospitals, including oxidative stress protection, biocide resistance mechanisms, and biofilm formation. In addition, we have demonstrated that both the formation and movement of type IV pili play an important role inA. baumanniibiofilm.IMPORTANCEAcinetobacter baumanniiis the causative agent of hospital-acquired infections, including pneumonia and serious blood and wound infections.A. baumanniiis an emerging pathogen and has become a threat to public health because it quickly develops antibiotic resistance, making treatment difficult or impossible. While the threat ofA. baumanniiis well recognized, our understanding of even its most basic biology lags behind. Analysis ofA. baumanniicellular functions to identify potential targets for drug development has stalled due in part to laborious genetic techniques. Here we have pioneered a novel recombineering system that facilitates efficient genome editing inA. baumanniiby single PCR products. This technology allows for rapid genome editing to quickly ascertain gene-phenotype relationships. To demonstrate the power of recombineering in dissectingA. baumanniibiology, we use this system to establish key gene-phenotype relationships important to infection and persistence in hospitals, including oxidative stress protection, biocide resistance, and biofilm formation.

scholarly journals ThecopYAZOperon Functions in Copper Efflux, Biofilm Formation, Genetic Transformation, and Stress Tolerance in Streptococcus mutans

2015 ◽  
Vol 197 (15) ◽  
pp. 2545-2557 ◽  
Author(s):  
Kamna Singh ◽  
Dilani B. Senadheera ◽  
Céline M. Lévesque ◽  
Dennis G. Cvitkovitch
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Genetic Transformation ◽  
Stress Tolerance ◽  
Biofilm Formation ◽  
Copper Homeostasis ◽  
Copper Stress ◽  
Wild Type ◽  
Genetic Competence ◽  
Content Type

ABSTRACTIn bacteria, copper homeostasis is closely monitored to ensure proper cellular functions while avoiding cell damage. Most Gram-positive bacteria utilize thecopYABZoperon for copper homeostasis, wherecopAandcopBencode copper-transporting P-type ATPases, whereascopYandcopZregulate the expression of thecopoperon.Streptococcus mutansis a biofilm-forming oral pathogen that harbors a putative copper-transportingcopYAZoperon. Here, we characterized the role ofcopYAZoperon in the physiology ofS. mutansand delineated the mechanisms of copper-induced toxicity in this bacterium. We observed that copper induced toxicity inS. mutanscells by generating oxidative stress and disrupting their membrane potential. Deletion of thecopYAZoperon inS. mutansstrain UA159 resulted in reduced cell viability under copper, acid, and oxidative stress relative to the viability of the wild type under these conditions. Furthermore, the ability ofS. mutansto form biofilms and develop genetic competence was impaired under copper stress. Briefly, copper stress significantly reduced cell adherence and total biofilm biomass, concomitantly repressing the transcription of thegtfB,gtfC,gtfD,gbpB, andgbpCgenes, whose products have roles in maintaining the structural and/or functional integrity of theS. mutansbiofilm. Furthermore, supplementation with copper or loss ofcopYAZresulted in significant reductions in transformability and in the transcription of competence-associated genes. Copper transport assays revealed that the ΔcopYAZstrain accrued significantly large amounts of intracellular copper compared with the amount of copper accumulation in the wild-type strain, thereby demonstrating a role for CopYAZ in the copper efflux ofS. mutans. The complementation of the CopYAZ system restored copper expulsion, membrane potential, and stress tolerance in thecopYAZ-null mutant. Taking these results collectively, we have established the function of theS. mutansCopYAZ system in copper export and have further expanded knowledge on the importance of copper homeostasis and the CopYAZ system in modulating streptococcal physiology, including stress tolerance, membrane potential, genetic competence, and biofilm formation.IMPORTANCES. mutansis best known for its role in the initiation and progression of human dental caries, one of the most common chronic diseases worldwide.S. mutansis also implicated in bacterial endocarditis, a life-threatening inflammation of the heart valve. The core virulence factors ofS. mutansinclude its ability to produce and sustain acidic conditions and to form a polysaccharide-encased biofilm that provides protection against environmental insults. Here, we demonstrate that the addition of copper and/or deletion ofcopYAZ(the copper homeostasis system) have serious implications in modulating biofilm formation, stress tolerance, and genetic transformation inS. mutans. Manipulating the pathways affected by copper and thecopYAZsystem may help to develop potential therapeutics to preventS. mutansinfection in and beyond the oral cavity.

scholarly journals Roles of Four Putative DEAD-Box RNA Helicase Genes in Growth of Listeria monocytogenes EGD-e under Heat, pH, Osmotic, Ethanol, and Oxidative Stress Conditions

2012 ◽  
Vol 78 (19) ◽  
pp. 6875-6882 ◽  
Author(s):  
Annukka Markkula ◽  
Miia Lindström ◽  
Per Johansson ◽  
Johanna Björkroth ◽  
Hannu Korkeala
Keyword(s):  
Oxidative Stress ◽  
Listeria Monocytogenes ◽  
Stress Tolerance ◽  
Deletion Mutant ◽  
Rna Helicase ◽  
Wild Type ◽  
Content Type ◽  
Oxidative Stresses ◽  
Dead Box ◽  
Mutant Strains

ABSTRACTTo examine the role of the four putative DEAD-box RNA helicase genes ofListeria monocytogenesEGD-e in stress tolerance, the growth of the Δlmo0866, Δlmo1246, Δlmo1450, and Δlmo1722deletion mutant strains at 42.5°C, at pH 5.6 or pH 9.4, in 6% NaCl, in 3.5% ethanol, and in 5 mM H2O2was studied. Restricted growth of the Δlmo0866deletion mutant strain in 3.5% ethanol suggests that Lmo0866 contributes to ethanol stress tolerance ofL. monocytogenesEGD-e. The Δlmo1450mutant strain showed negligible growth at 42.5°C, at pH 9.4, and in 5 mM H2O2and a lower maximum growth temperature than the wild-type EGD-e, suggesting that Lmo1450 is involved in the tolerance ofL. monocytogenesEGD-e to heat, alkali, and oxidative stresses. The altered stress tolerance of the Δlmo0866and Δlmo1450deletion mutant strains did not correlate with changes in relative expression levels oflmo0866andlmo1450genes under corresponding stresses, suggesting that Lmo0866- and Lmo1450-dependent tolerance to heat, alkali, ethanol, or oxidative stress is not regulated at the transcriptional level. Growth of the Δlmo1246and Δlmo1722deletion mutant strains did not differ from that of the wild-type EGD-e under any of the conditions tested, suggesting that Lmo1246 and Lmo1722 have no roles in the growth ofL. monocytogenesEGD-e under heat, pH, osmotic, ethanol, or oxidative stress. This study shows that the putative DEAD-box RNA helicase geneslmo0866andlmo1450play important roles in tolerance ofL. monocytogenesEGD-e to ethanol, heat, alkali, and oxidative stresses.

scholarly journals NrdH Redoxin Enhances Resistance to Multiple Oxidative Stresses by Acting as a Peroxidase Cofactor in Corynebacterium glutamicum

2013 ◽  
Vol 80 (5) ◽  
pp. 1750-1762 ◽  
Author(s):  
Mei-Ru Si ◽  
Lei Zhang ◽  
Zhi-Fang Yang ◽  
Yi-Xiang Xu ◽  
Ying-Bao Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Corynebacterium Glutamicum ◽  
Sequence Similarity ◽  
Thioredoxin Reductase ◽  
Amino Acid Sequence Similarity ◽  
Content Type ◽  
Reduction Activity ◽  
Oxidative Stresses ◽  
High Amino Acid ◽  
Thiol Peroxidase

ABSTRACTNrdH redoxins are small protein disulfide oxidoreductases behaving like thioredoxins but sharing a high amino acid sequence similarity to glutaredoxins. Although NrdH redoxins are supposed to be another candidate in the antioxidant system, their physiological roles in oxidative stress remain unclear. In this study, we confirmed that theCorynebacterium glutamicumNrdH redoxin catalytically reduces the disulfides in the class Ib ribonucleotide reductases (RNR), insulin and 5,5′-dithiobis-(2-nitrobenzoic acid) (DTNB), by exclusively receiving electrons from thioredoxin reductase. Overexpression of NrdH increased the resistance ofC. glutamicumto multiple oxidative stresses by reducing ROS accumulation. Accordingly, elevated expression of thenrdHgene was observed when theC. glutamicumwild-type strain was exposed to oxidative stress conditions. It was discovered that the NrdH-mediated resistance to oxidative stresses was largely dependent on the presence of the thiol peroxidase Prx, as the increased resistance to oxidative stresses mediated by overexpression of NrdH was largely abrogated in theprxmutant. Furthermore, we showed that NrdH facilitated the hydroperoxide reduction activity of Prx by directly targeting and serving as its electron donor. Thus, we present evidence that the NrdH redoxin can protect against the damaging effects of reactive oxygen species (ROS) induced by various exogenous oxidative stresses by acting as a peroxidase cofactor.

scholarly journals Stress Survival Islet 2, Predominantly Present in Listeria monocytogenes Strains of Sequence Type 121, Is Involved in the Alkaline and Oxidative Stress Responses

2017 ◽  
Vol 83 (16) ◽  
Author(s):  
Eva Harter ◽  
Eva Maria Wagner ◽  
Andreas Zaiser ◽  
Sabrina Halecker ◽  
Martin Wagner ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Listeria Monocytogenes ◽  
Stress Responses ◽  
Food Processing ◽  
Stress Conditions ◽  
Content Type ◽  
Oxidative Stresses ◽  
Stress Survival ◽  
Oxidative Stress Responses ◽  
And Oxidative Stress

ABSTRACT The foodborne pathogen Listeria monocytogenes is able to survive a variety of stress conditions leading to the colonization of different niches like the food processing environment. This study focuses on the hypervariable genetic hot spot lmo0443 to lmo0449 haboring three inserts: the stress survival islet 1 (SSI-1), the single-gene insert LMOf2365_0481, and two homologous genes of the nonpathogenic species Listeria innocua: lin0464, coding for a putative transcriptional regulator, and lin0465, encoding an intracellular PfpI protease. Our prevalence study revealed a different distribution of the inserts between human and food-associated isolates. The lin0464-lin0465 insert was predominantly found in food-associated strains of sequence type 121 (ST121). Functional characterization of this insert showed that the putative PfpI protease Lin0465 is involved in alkaline and oxidative stress responses but not in acidic, gastric, heat, cold, osmotic, and antibiotic stresses. In parallel, deletion of lin0464 decreased survival under alkaline and oxidative stresses. The expression of both genes increased significantly under oxidative stress conditions independently of the alternative sigma factor σB. Furthermore, we showed that the expression of the protease gene lin0465 is regulated by the transcription factor lin0464 under stress conditions, suggesting that lin0464 and lin0465 form a functional unit. In conclusion, we identified a novel stress survival islet 2 (SSI-2), predominantly present in L. monocytogenes ST121 strains, beneficial for survival under alkaline and oxidative stresses, potentially supporting adaptation and persistence of L. monocytogenes in food processing environments. IMPORTANCE Listeria monocytogenes strains of ST121 are known to persist for months and even years in food processing environments, thereby increasing the risk of food contamination and listeriosis. However, the molecular mechanism underlying this remarkable niche-specific adaptation is still unknown. Here, we demonstrate that the genomic islet SSI-2, predominantly present in L. monocytogenes ST121 strains, is beneficial for survival under alkaline and oxidative stress conditions, which are routinely encountered in food processing environments. Our findings suggest that SSI-2 is part of a diverse set of molecular determinants contributing to niche-specific adaptation and persistence of L. monocytogenes ST121 strains in food processing environments.

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