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Abstract Background As a major threat to the oyster industry, Pacific Oyster Mortality Syndrome (POMS) is a polymicrobial disease affecting the main oyster species farmed across the world. POMS affects oyster juveniles and became panzootic this last decade, but POMS resistance in some oyster genotypes has emerged. While we know some genetic loci associated with resistance, the underlying mechanisms remained uncharacterized. So, we developed a comparative transcriptomic approach using basal gene expression profiles between different oyster biparental families with contrasted phenotypes when confronted to POMS (resistant or susceptible). Results We showed that POMS resistant oysters show differential expression of genes involved in stress responses, protein modifications, maintenance of DNA integrity and repair, and immune and antiviral pathways. We found similarities and clear differences among different molecular pathways in the different resistant families. These results suggest that the resistance process is polygenic and partially varies according to the oyster genotype. Conclusions We found differences in basal expression levels of genes related to TLR-NFκB, JAK-STAT and STING-RLR pathways. These differences could explain the best antiviral response, as well as the robustness of resistant oysters when confronted to POMS. As some of these genes represent valuable candidates for selective breeding, we propose future studies should further examine their function.

Background: As a major threat to the oyster industry, Pacific Oyster Mortality Syndrome (POMS) is a polymicrobial disease affecting the main oyster species farmed across the world. POMS affects oyster juveniles and became panzootic this last decade, but POMS resistance in some oyster genotypes has emerged. While we know some genetic loci associated with resistance, the underlying mechanisms remained uncharacterized. So, we developed a comparative transcriptomic approach using basal gene expression profiles between different oyster biparental families with contrasted phenotypes when confronted to POMS (resistant or susceptible). Results: We showed that POMS resistant oysters show differential expression of genes involved in stress responses, protein modifications, maintenance of DNA integrity and repair, and immune and antiviral pathways. We found similarities and clear differences among different molecular pathways in the different resistant families. These results suggest that the resistance process is polygenic and partially varies according to the oyster genotype. Conclusions: We found differences in basal expression levels of genes related to TLR-NFκB, JAK-STAT and STING-RLR pathways. These differences could explain the best antiviral response, as well as the robustness of resistant oysters when confronted to POMS. As some of these genes represent valuable candidates for selective breeding, we propose future studies should further examine their function. [ABSTRACT FROM AUTHOR]

Phaeobacter inhibens S4Sm acts as a probiotic bacterium against the oyster pathogen, Vibrio coralliilyticus. Here we report that P. inhibens S4Sm secretes three molecules that down regulate transcription of major virulence factors, metalloprotease genes, in V. coralliilyticus cultures. The effects of S4Sm culture supernatant on the transcription of three genes involved in protease activity, vcpA, vcpB, and vcpR (encoding metalloproteases A and B and their transcriptional regulator, respectively), were examined by qRT-PCR. Expression of vcpB and vcpR were reduced to 36% and 6.6%, respectively, compared to an untreated control. We constructed a V. coralliilyticus GFP-reporter strain to detect the activity of inhibitory compounds. Using a bioassay-guided approach, the molecules responsible for V. coralliilyticus protease inhibition activity were isolated from S4Sm supernatant and identified as three N-acyl homoserine lactones (AHLs). The three AHLs are N-(3-hydroxydecanoyl)-L homoserine lactone, N-(dodecanoyl-2,5-diene)-L-homoserine lactone and N-(3-hydroxytetradecanoyl-7-ene)-L-homoserine lactone, and their half maximal inhibitory concentrations (IC50) against V. coralliilyticus protease activity are 0.26 μM, 3.7 μM and 2.9 μM, respectively. Our qRT-PCR data demonstrated that exposure to the individual AHLs reduced transcription of vcpR and vcpB. Combinations of the three AHLs (any two or all three AHLs) on V. coralliilyticus showed additive effects upon protease inhibition activity. These AHL compounds may contribute to the host protective effects of S4Sm by disrupting the quorum-sensing pathway that activates protease transcription of V. coralliilyticus. [ABSTRACT FROM AUTHOR]

The marine bacterium Labrenzia sp. strain 011 was isolated from the coastal sediment of Kronsgaard, Germany. The Labrenzia species are suggested to be protective agents of mollusks. Labrenzia sp. strain 011 produces specialized metabolites, which showed activity against a range of microorganisms, thereunder strong inhibitory effects against Pseudoroseovarius crassostreae DSM 16,950 (genus Roseovarius), the causative agent of oyster disease. The genome of Labrenzia sp. strain 011 was sequenced and assembled into 65 contigs, has a size of 5.1 Mbp, and a G+C content of 61.6%. A comparative genome analysis defined Labrenzia sp. strain 011 as a distinct new species within the genus Labrenzia, whereby 44% of the genome was contributed to the Labrenzia core genome. The genomic data provided here is expected to contribute to a deeper understanding of the mollusk-protective role of Labrenzia spp.

Background: The probiotic bacterium Phaeobacter inhibens strain S4Sm, isolated from the inner shell surface of a healthy oyster, secretes the antibiotic tropodithietic acid (TDA), is an excellent biofilm former, and increases oyster larvae survival when challenged with bacterial pathogens. In this study, we investigated the specific roles of TDA secretion and biofilm formation in the probiotic activity of S4Sm. Results: Mutations in clpX (ATP-dependent ATPase) and exoP (an exopolysaccharide biosynthesis gene) were created by insertional mutagenesis using homologous recombination. Mutation of clpX resulted in the loss of TDA production, no decline in biofilm formation, and loss of the ability to inhibit the growth of Vibrio tubiashii and Vibrio anguillarum in co-colonization experiments. Mutation of exoP resulted in a ~60 % decline in biofilm formation, no decline in TDA production, and delayed inhibitory activity towards Vibrio pathogens in co-colonization experiments. Both clpX and exoP mutants exhibited reduced ability to protect oyster larvae from death when challenged by Vibrio tubiashii. Complementation of the clpX and exoP mutations restored the wild type phenotype. We also found that pre-colonization of surfaces by S4Sm was critical for this bacterium to inhibit pathogen colonization and growth. Conclusions: Our observations demonstrate that probiotic activity by P. inhibens S4Sm involves contributions from both biofilm formation and the production of the antibiotic TDA. Further, probiotic activity also requires colonization of surfaces by S4Sm prior to the introduction of the pathogen. [ABSTRACT FROM AUTHOR]

The article presents a study which discusses the failure to sustain oyster fisheries and the dramatic decline in the population of the eastern oyster Crassostrea virginica in many U.S. Atlantic and Gulf of Mexico estuaries. It mentions that oysters offer significant ecosystem services which led state management agencies to allow oyster reefs to be degraded and mined to extract the marketable oysters. It relates that examinations on the estuaries are considered successful from an ecological or oyster fishery view, but success on its restoration of subtidal reefs varies.

Phaeobacter inhibens S4Sm acts as a probiotic bacterium against the oyster pathogen Vibrio coralliilyticus Here, we report that P. inhibens S4Sm secretes three molecules that downregulate the transcription of major virulence factors, metalloprotease genes, in V. coralliilyticus cultures. The effects of the S4Sm culture supernatant on the transcription of three genes involved in protease activity, namely, vcpA , vcpB , and vcpR (encoding metalloproteases A and B and their transcriptional regulator, respectively), were examined by reverse transcriptase quantitative PCR (qRT-PCR). The expression of vcpB and vcpR were reduced to 36% and 6.6%, respectively, compared to that in an untreated control. We constructed a V. coralliilyticus green fluorescent protein (GFP) reporter strain to detect the activity of inhibitory compounds. Using a bioassay-guided approach, the molecules responsible for V. coralliilyticus protease inhibition activity were isolated from S4Sm supernatant and identified as three N -acyl homoserine lactones (AHLs). The three AHLs are N -(3-hydroxydecanoyl)-l-homoserine lactone, N -(dodecanoyl-2,5-diene)-l-homoserine lactone, and N -(3-hydroxytetradecanoyl-7-ene)-l-homoserine lactone, and their half maximal inhibitory concentrations (IC 50 s) against V. coralliilyticus protease activity were 0.26 μM, 3.7 μM, and 2.9 μM, respectively. Our qRT-PCR data demonstrated that exposures to the individual AHLs reduced the transcription of vcpR and vcpB Combinations of the three AHLs (any two or all three AHLs) on V. coralliilyticus produced additive effects on protease inhibition activity. These AHL compounds may contribute to the host protective effects of S4Sm by disrupting the quorum sensing pathway that activates protease transcription of V. coralliilyticus IMPORTANCE Probiotics represent a promising alternative strategy to control infection and disease caused by marine pathogens of aquaculturally important species. Generally, the beneficial effects of probiotics include improved water quality, control of pathogenic bacteria and their virulence, stimulation of the immune system, and improved animal growth. Previously, we isolated a probiotic bacterium, Phaeobacter inhibens S4Sm, which protects oyster larvae from Vibrio coralliilyticus RE22Sm infection. We also demonstrated that both antibiotic secretion and biofilm formation play important roles in S4Sm probiotic activity. Here, we report that P. inhibens S4Sm, an alphaproteobacterium and member of the Roseobacter clade, also secretes secondary metabolites that hijack the quorum sensing ability of V. coralliilyticus RE22Sm, suppressing virulence gene expression. This finding demonstrates that probiotic bacteria can exert their host protection by using a multipronged array of behaviors that limit the ability of pathogens to become established and cause infection., (Copyright © 2019 American Society for Microbiology.)

Background: The probiotic bacterium Phaeobacter inhibens strain S4Sm, isolated from the inner shell surface of a healthy oyster, secretes the antibiotic tropodithietic acid (TDA), is an excellent biofilm former, and increases oyster larvae survival when challenged with bacterial pathogens. In this study, we investigated the specific roles of TDA secretion and biofilm formation in the probiotic activity of S4Sm. Results: Mutations in clpX (ATP-dependent ATPase) and exoP (an exopolysaccharide biosynthesis gene) were created by insertional mutagenesis using homologous recombination. Mutation of clpX resulted in the loss of TDA production, no decline in biofilm formation, and loss of the ability to inhibit the growth of Vibrio tubiashii and Vibrio anguillarum in co-colonization experiments. Mutation of exoP resulted in a ~60 % decline in biofilm formation, no decline in TDA production, and delayed inhibitory activity towards Vibrio pathogens in co-colonization experiments. Both clpX and exoP mutants exhibited reduced ability to protect oyster larvae from death when challenged by Vibrio tubiashii. Complementation of the clpX and exoP mutations restored the wild type phenotype. We also found that pre-colonization of surfaces by S4Sm was critical for this bacterium to inhibit pathogen colonization and growth. Conclusions: Our observations demonstrate that probiotic activity by P. inhibens S4Sm involves contributions from both biofilm formation and the production of the antibiotic TDA. Further, probiotic activity also requires colonization of surfaces by S4Sm prior to the introduction of the pathogen. Electronic supplementary material The online version of this article (doi:10.1186/s12866-015-0617-z) contains supplementary material, which is available to authorized users.