<i>Serratia marcescens</i> Gene Required for Surfactant Serrawettin W1 Production Encodes Putative Aminolipid Synthetase Belonging to Nonribosomal Peptide Synthetase Family

Li, Hong; Tanikawa, Taichiro; Sato, Yohei; Nakagawa, Yasuaki; Matsuyama, Tohey

doi:10.1111/j.1348-0421.2005.tb03734.x

Cited by 64 publications

(49 citation statements)

References 29 publications

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“…As a first approach to identifying L. pneumophila genes that promote surfactant production, we examined the genome database of strain 130b (87) for a gene(s) that is predicted to encode a protein with sequence similarity to a bacterial enzyme known to be involved in the synthesis of a surfactant. The open reading frame (ORF) lpw_23601 was predicted to encode a product sharing 30% amino acid (aa) identity (E value ϭ 2 ϫ 10 Ϫ61 ) with serrawettin W1 synthetase; serrawettin is a surfactant produced by S. marcescens (59). Using allelic exchange, we isolated two mutants lacking lpw_23601 but found that both produced normal levels of a surfactant and surface translocation (see Fig.…”

Section: Resultsmentioning

confidence: 99%

The Surfactant of Legionella pneumophila Is Secreted in a TolC-Dependent Manner and Is Antagonistic toward Other Legionella Species

2011

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When Legionella pneumophila grows on agar plates, it secretes a surfactant that promotes flagellum-and pilus-independent "sliding" motility. We isolated three mutants that were defective for surfactant. The first two had mutations in genes predicted to encode cytoplasmic enzymes involved in lipid metabolism. These genes mapped to two adjacent operons that we designated bbcABCDEF and bbcGHIJK. Backcrossing and complementation confirmed the importance of the bbc genes and suggested that the Legionella surfactant is lipid containing. The third mutant had an insertion in tolC. TolC is the outer membrane part of various trimolecular complexes involved in multidrug efflux and type I protein secretion. Complementation of the tolC mutant restored sliding motility. Mutants defective for an inner membrane partner of TolC also lacked a surfactant, confirming that TolC promotes surfactant secretion. L. pneumophila (lspF) mutants lacking type II protein secretion (T2S) are also impaired for a surfactant. When the tolC and lspF mutants were grown next to each other, the lsp mutant secreted surfactant, suggesting that TolC and T2S conjoin to mediate surfactant secretion, with one being the conduit for surfactant export and the other the exporter of a molecule that is required for induction or maturation of surfactant synthesis/secretion. Although the surfactant was not required for the extracellular growth, intracellular infection, and intrapulmonary survival of L. pneumophila, it exhibited antimicrobial activity toward seven other species of Legionella but not toward various nonLegionella species. These data suggest that the surfactant provides L. pneumophila with a selective advantage over other legionellae in the natural environment.

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Section: Resultsmentioning

confidence: 99%

The Surfactant of Legionella pneumophila Is Secreted in a TolC-Dependent Manner and Is Antagonistic toward Other Legionella Species

2011

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“…Surfactant production and flagellar expression are regulated by different genes and environmental signals. The sliding hypothesis can be tested with mutant strains defective in surfactant production (21). Interestingly, Pseudomonas putida bacteria lacking flagella lose their ability to migrate along hyphae, suggesting that unlike S. marcescens, they rely entirely on flagella to move along the fungal mycelium (22).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Bacterial (Serratia marcescens) Attachment to, Migration along, and Killing of Fungal Hyphae

Hover

Maya

Ron

et al. 2016

Appl Environ Microbiol

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We have found a remarkable capacity for the ubiquitous Gram-negative rod bacterium Serratia marcescens to migrate along and kill the mycelia of zygomycete molds. This migration was restricted to zygomycete molds and several basidiomycete species. No migration was seen on any molds of the phylum Ascomycota. S. marcescens migration did not require fungal viability or surrounding growth medium, as bacteria migrated along aerial hyphae as well. S. marcescens did not exhibit growth tropism toward zygomycete mycelium. Bacterial migration along hyphae proceeded only when the hyphae grew into the bacterial colony. S. marcescens cells initially migrated along the hyphae, forming attached microcolonies that grew and coalesced to generate a biofilm that covered and killed the mycelium. Flagellum-defective strains of S. marcescens were able to migrate along zygomycete hyphae, although they were significantly slower than the wild-type strain and were delayed in fungal killing. Bacterial attachment to the mycelium does not necessitate type 1 fimbrial adhesion, since mutants defective in this adhesin migrated equally well as or faster than the wild-type strain. Killing does not depend on the secretion of S. marcescens chitinases, as mutants in which all three chitinase genes were deleted retained wild-type killing abilities. A better understanding of the mechanisms by which S. marcescens binds to, spreads on, and kills fungal hyphae might serve as an excellent model system for such interactions in general; fungal killing could be employed in agricultural fungal biocontrol.

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“…Foam formation creates potential for microbial contamination, leads to the need for addition of large amounts of antifoam agent, and decreases bacterial activity. Previous reports showed that three serrawettins (serrawettin W1, W2, and W3) were produced by S. marcescens [7]. Each serrawettin produced by respective S. marcescens strains is restricted to one molecular species (e.g., W1 from strain 274, ATCC 13880; W2 from strain NS 25; and W3 from strain NS 45) [7,10].…”

Section: Introductionmentioning

confidence: 99%

Microbial production of 2,3-butanediol by a surfactant (serrawettin)-deficient mutant of Serratia marcescens H30

Zhang¹,

Sun²,

Ye³

et al. 2010

J Ind Microbiol Biotechnol

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Serrawettin W1 produced by Serratia marcescens is a surface-active exolipid resulting in a lot foam formation during the 2,3-butanediol (2,3-BD) fermentation process. In order to avoid excessive addition of antifoam agent and microbial contamination, S. marcescens mutants deficient in serrawettin W1 formation were successfully constructed through insertional inactivation of the swrW gene coding for serrawettin W1 synthase. The shake flask and batch experiments suggested that disruption of the swrW gene led to significant reduction of the foam formation and improved 2,3-BD production a little. Ultimately, fed-batch culturing of the mutant afforded a maximum 2,3-BD concentration of 152 g l(-1) with a productivity of 2.67 g l(-1) h(-1) and a yield of 92.6% at 57 h.

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Serratia marcescens Gene Required for Surfactant Serrawettin W1 Production Encodes Putative Aminolipid Synthetase Belonging to Nonribosomal Peptide Synthetase Family

Cited by 64 publications

References 29 publications

The Surfactant of Legionella pneumophila Is Secreted in a TolC-Dependent Manner and Is Antagonistic toward Other Legionella Species

The Surfactant of Legionella pneumophila Is Secreted in a TolC-Dependent Manner and Is Antagonistic toward Other Legionella Species

Mechanisms of Bacterial (Serratia marcescens) Attachment to, Migration along, and Killing of Fungal Hyphae

Microbial production of 2,3-butanediol by a surfactant (serrawettin)-deficient mutant of Serratia marcescens H30

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