Responses of Lactic Acid Bacteria to Heavy Metal Stress

Solioz, Marc; Mermod, Mélanie; Abicht, Helge K.; Mancini, Stefano

doi:10.1007/978-0-387-92771-8_9

Cited by 22 publications

(23 citation statements)

References 188 publications

(178 reference statements)

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“…Ethanol stress is of particular importance mainly for Oenococcus oeni, which performs malolactic fermentation (MLF) during wine making. There are also stresses that have gained momentum rather recently, such as metal stress (26). During acidification, LAB may cause the solubilization of metals, which may be toxic depending on their concentration.…”

Section: Common Stresses Encountered By Lab In Their Ecological Nichesmentioning

confidence: 99%

“…Characterized LAB copper sensors include the CopZ-type copper chaperones and the CopY-type regulators (26). For Enterococcus hirae, it has been proposed that CopZ binds cytoplasmic Cu ϩ and transfers it to CopB for transporter-mediated export and to the CopY regulator for signaling (26) (Fig.…”

Section: One-component Systemsmentioning

confidence: 99%

“…1). CopY is an OCS with an N-terminal DNA-binding domain and a C-terminal metal-binding domain (26). At a low Cu ϩ concentration, Zn 2ϩ occupies the metal-binding site of CopY and the protein is bound to its target sequence, thereby inhibiting cop operon expression.…”

Section: One-component Systemsmentioning

confidence: 99%

“…When the Cu ϩ concentration increases, Cu ϩ -CopZ transfers its copper ion to CopY, displacing Zn 2ϩ from the metal-binding site and resulting in CopY release from the DNA. This allows transcription of the cop operon (26). The Lc.…”

Section: One-component Systemsmentioning

confidence: 99%

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Stress Physiology of Lactic Acid Bacteria

Papadimitriou

Alegría

Bron

et al. 2016

Microbiol Mol Biol Rev

539

404

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SUMMARYLactic acid bacteria (LAB) are important starter, commensal, or pathogenic microorganisms. The stress physiology of LAB has been studied in depth for over 2 decades, fueled mostly by the technological implications of LAB robustness in the food industry. Survival of probiotic LAB in the host and the potential relatedness of LAB virulence to their stress resilience have intensified interest in the field. Thus, a wealth of information concerning stress responses exists today for strains as diverse as starter (e.g.,Lactococcus lactis), probiotic (e.g., severalLactobacillusspp.), and pathogenic (e.g.,EnterococcusandStreptococcusspp.) LAB. Here we present the state of the art for LAB stress behavior. We describe the multitude of stresses that LAB are confronted with, and we present the experimental context used to study the stress responses of LAB, focusing on adaptation, habituation, and cross-protection as well as on self-induced multistress resistance in stationary phase, biofilms, and dormancy. We also consider stress responses at the population and single-cell levels. Subsequently, we concentrate on the stress defense mechanisms that have been reported to date, grouping them according to their direct participation in preserving cell energy, defending macromolecules, and protecting the cell envelope. Stress-induced responses of probiotic LAB and commensal/pathogenic LAB are highlighted separately due to the complexity of the peculiar multistress conditions to which these bacteria are subjected in their hosts. Induction of prophages under environmental stresses is then discussed. Finally, we present systems-based strategies to characterize the “stressome” of LAB and to engineer new food-related and probiotic LAB with improved stress tolerance.

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Section: Common Stresses Encountered By Lab In Their Ecological Nichesmentioning

confidence: 99%

Section: One-component Systemsmentioning

confidence: 99%

Section: One-component Systemsmentioning

confidence: 99%

Section: One-component Systemsmentioning

confidence: 99%

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Stress Physiology of Lactic Acid Bacteria

Papadimitriou

Alegría

Bron

et al. 2016

Microbiol Mol Biol Rev

539

404

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“…Inside the cell, specialized proteins are responsible for copper handling, such as insertion into cuproenzymes or delivery to copper-responsive regulators [for recent reviews, see Solioz et al (2010) and Magnani & Solioz (2007)]. To the extent it has been studied, these copper homeostatic proteins bind Cu + and it is generally assumed that Cu + prevails in the reducing environment of the cytoplasm, without the need for a copper reductase (Solioz et al, 2011). A key element of copper homeostasis in all bacteria is the coppertransporting ATPase.…”

Section: Introductionmentioning

confidence: 99%

Non-enzymic copper reduction by menaquinone enhances copper toxicity in Lactococcus lactis IL1403

et al. 2013

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Lactococcus lactis possesses a pronounced extracellular Cu 2+ -reduction activity which leads to the accumulation of Cu + in the medium. The kinetics of this reaction were not saturable by increasing copper concentrations, suggesting a non-enzymic reaction. A copper-reductasedeficient mutant, isolated by random transposon mutagenesis, had an insertion in the menE gene, which encodes O-succinylbenzoic acid CoA ligase. This is a key enzyme in menaquinone biosynthesis. The DmenE mutant was deficient in short-chain menaquinones, and exogenously added menaquinone complemented the copper-reductase-deficient phenotype. Haem-induced respiration of wild-type L. lactis efficiently suppressed copper reduction, presumably by competition by the bd-type quinol oxidase for menaquinone. As expected, the DmenE mutant was respiration-deficient, but could be made respiration-proficient by supplementation with menaquinone. Growth of wild-type cells was more copper-sensitive than that of the DmenE mutant, due to the production of Cu + ions by the wild-type. This growth inhibition of the wild-type was strongly attenuated if Cu + was scavenged with the Cu(I) chelator bicinchoninic acid. These findings support a model whereby copper is non-enzymically reduced at the membrane by menaquinones. Respiration effectively competes for reduced quinones, which suppresses copper reduction. These findings highlight novel links between copper reduction, respiration and Cu + toxicity in L. lactis.

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