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The involvement of the Type Six Secretion System (T6SS) in the virulence of Ralstonia solanacearum on brinjal.

ABSTRACT: Ralstonia solanacearum is an important soil-borne plant pathogen which causes bacterial wilt in a large number of crops. Bacterial Type Six Secretion System (T6SS) is known to participate in pathogenesis, bacterial interaction and inter-bacterial competition. Contribution of T6SS in the virulence of R. solanacearum on eggplant (Solanum melongena L) is studied. In this study, five T6SS gene (ompA, vgrG3, hcp, tssH and tssM) mutants have been developed by insertional mutagenesis and the virulence of the mutants was evaluated on eggplant. In general, the T6SS mutants showed significant reduction of wilt on eggplant. R. solanacearum mutant of ompA gene significantly reduced the wilt from day five through day eight in petiole inoculation. In soil drench inoculation, R. solanacearum mutant of vgrG3 gene reduced the wilt on eggplant and was significantly different throughout the experimental period. Other mutants, viz., tssH, tssM and hcp, also reduced the wilt during the initial stages of disease development. This is the first report on the role of T6SS genes, ompA, vgrG3, hcp and tssH on virulence of R. solanacearum.

SUBMITTER: Asolkar T

PROVIDER: S-EPMC7324442 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Integrated regulation of the type III secretion system and other virulence determinants in Ralstonia solanacearum.

Project description:In many plant and animal bacterial pathogens, the Type III secretion system (TTSS) that directly translocates effector proteins into the eukaryotic host cells is essential for the development of disease. In all species studied, the transcription of the TTSS and most of its effector substrates is tightly regulated by a succession of consecutively activated regulators. However, the whole genetic programme driven by these regulatory cascades is still unknown, especially in bacterial plant pathogens. Here, we have characterised the programme triggered by HrpG, a host-responsive regulator of the TTSS activation cascade in the plant pathogen Ralstonia solanacearum. We show through genome-wide expression analysis that, in addition to the TTSS, HrpG controls the expression of a previously undescribed TTSS-independent pathway that includes a number of other virulence determinants and genes likely involved in adaptation to life in the host. Functional studies revealed that this second pathway co-ordinates the bacterial production of plant cell wall-degrading enzymes, exopolysaccharide, and the phytohormones ethylene and auxin. We provide experimental evidence that these activities contribute to pathogenicity. We also show that the ethylene produced by R. solanacearum is able to modulate the expression of host genes and can therefore interfere with the signalling of plant defence responses. These results provide a new, integrated view of plant bacterial pathogenicity, where a common regulator activates synchronously upon infection the TTSS, other virulence determinants and a number of adaptive functions, which act co-operatively to cause disease.

| S-EPMC1557829 | biostudies-literature

Involvement of a PadR regulator PrhP on virulence of Ralstonia solanacearum by controlling detoxification of phenolic acids and type III secretion system.

Project description:Ralstonia solanacearum can metabolize ferulic acid (FA) and salicylic acid (SA), two representative phenolic acids, to protect it from toxicity of phenolic acids. Here, we genetically demonstrated a novel phenolic acid decarboxylase regulator (PadR)-like regulator PrhP as a positive regulator on detoxification of SA and FA in R. solanacearum. Although the ability to degrade SA and FA enhances the infection process of R. solanacearum toward host plants, PrhP greatly contributes to the infection process besides degradation of SA and FA. Our results from the growth assay, promoter activity assay, RNA-seq and qRT-PCR revealed that PrhP plays multiple roles in the virulence of R. solanacearum: (1) positively regulates expression of genes for degradation of SA and FA; (2) positively regulates expression of genes encoding type III secretion system (T3SS) and type III effectors both in vitro and in planta; (3) positively regulates expression of many virulence-related genes, such as the flagella, type IV pili and cell wall degradation enzymes; and (4) is important for the extensive proliferation in planta. The T3SS is one of the essential pathogenicity determinants in many pathogenic bacteria, and PrhP positively regulates its expression mediated with the key regulator HrpB but through some novel pathway to HrpB in R. solanacearum. This is the first report on PadR regulators to regulate the T3SS and it could improve our understanding of the various biological functions of PadR regulators and the complex regulatory pathway on T3SS in R. solanacearum.

| S-EPMC6804342 | biostudies-literature

Oleanolic Acid Induces the Type III Secretion System of Ralstonia solanacearum.

Project description:Ralstonia solanacearum, the causal agent of bacterial wilt, can naturally infect a wide range of host plants. The type III secretion system (T3SS) is a major virulence determinant in this bacterium. Studies have shown that plant-derived compounds are able to inhibit or induce the T3SS in some plant pathogenic bacteria, though no specific T3SS inhibitor or inducer has yet been identified in R. solanacearum. In this study, a total of 50 different compounds were screened and almost half of them (22 of 50) significantly inhibited or induced the T3SS expression of R. solanacearum. Based on the strong induction activity on T3SS, the T3SS inducer oleanolic acid (OA) was chosen for further study. We found that OA induced the expression of T3SS through the HrpG-HrpB pathway. Some type III effector genes were induced in T3SS inducing medium supplemented with OA. In addition, OA targeted only the T3SS and did not affect other virulence determinants. Finally, we observed that induction of T3SS by OA accelerated disease progress on tobacco. Overall our results suggest that plant-derived compounds are an abundant source of R. solanacearum T3SS regulators, which could prove useful as tools to interrogate the regulation of this key virulence pathway.

| S-EPMC4686671 | biostudies-literature

A putative LysR-type transcriptional regulator PrhO positively regulates the type III secretion system and contributes to the virulence of Ralstonia solanacearum.

Project description:LysR-type transcriptional regulators (LTTRs) are ubiquitous and abundant amongst bacteria and control a variety of cellular processes. Here, we investigated the effect of Rsc1880 (a putative LTTR, hereafter designated as PrhO) on the pathogenicity of Ralstonia solanacearum. Deletion of prhO substantially reduced the expression of the type III secretion system (T3SS) both in vitro and in planta, and resulted in significantly impaired virulence in tomato and tobacco plants. Complementary prhO completely restored the reduced virulence and T3SS expression to that of the wild-type. Moreover, PrhO-dependent T3SS and virulence were conserved amongst R. solanacearum species. However, deletion of prhO did not alter biofilm formation, swimming mobility and in planta growth. The expression of some type III effectors was significantly reduced in prhO mutants, but the hypersensitive response was not affected in tobacco leaves. Consistent with the key regulatory role of HrpB on T3SS, PrhO positively regulated the T3SS through HrpB. Furthermore, PrhO regulated hrpB expression via two close paralogues, HrpG and PrhG, which are two-component response regulators and positively regulate hrpB expression in a parallel manner. However, deletion of prhO did not alter the expression of phcA, prhJ and prhN, which are also involved in hrpB regulation. In addition, PrhO was expressed in a cell density-dependent manner, but negatively repressed by itself. No regulation was observed for HrpB, PhcA and PrhN on prhO expression. Taken together, we genetically demonstrated that PrhO is a novel virulence regulator of R. solanacearum, which positively regulates T3SS expression through HrpG, PrhG and HrpB and contributes to virulence.

| S-EPMC6638147 | biostudies-literature

PrhN, a putative marR family transcriptional regulator, is involved in positive regulation of type III secretion system and full virulence of Ralstonia solanacearum.

Project description:The MarR-family of transcriptional regulators are involved in various cellular processes, including resistance to multiple antibiotics and other toxic chemicals, adaptation to different environments and pathogenesis in many plant and animal pathogens. Here, we reported a new MarR regulator PrhN, which was involved in the pathogenesis of Ralstonia solanacearum. prhN mutant exhibited significantly reduced virulence and stem colonization compared to that of wild type in tomato plants. prhN mutant caused identical hypersensitive response (HR) on resistant plants to the wild type. Deletion of prhN gene substantially reduced the expression of type III secretion system (T3SS) in vitro and in planta (mainly in tomato plants), which is essential for pathogenicity of R. solanacearum, and the complemented PrhN could restore its virulence and T3SS expression to that of wild type. T3SS is directly controlled by AraC-type transcriptional regulator HrpB, and the transcription of hrpB is activated by HrpG and PrhG. HrpG and PrhG are homologs but are regulated by the PhcA positively and negatively, respectively. Deletion of prhN gene also abolished the expression of hrpB and prhG, but didn't change the expression of hrpG and phcA. Together, these results indicated that PrhN positively regulates T3SS expression through PrhG and HrpB. PrhN and PhcA should regulate prhG expression in a parallel way. This is the first report on the pathogenesis of MarR regulator in R. solanacearum, and this new finding will improve our understanding on the various biological functions of MarR regulator and the complex regulatory network on hrp regulon in R. solanacearum.

| S-EPMC4412082 | biostudies-literature

Exposure to Umbelliferone Reduces <i>Ralstonia solanacearum</i> Biofilm Formation, Transcription of Type III Secretion System Regulators and Effectors and Virulence on Tobacco.

Project description:Ralstonia solanacearum is one of the most devastating phytopathogens and causes bacterial wilt, which leads to severe economic loss due to its worldwide distribution and broad host range. Certain plant-derived compounds (PDCs) can impair bacterial virulence by suppressing pathogenic factors of R. solanacearum. However, the inhibitory mechanisms of PDCs in bacterial virulence remain largely unknown. In this study, we screened a library of coumarins and derivatives, natural PDCs with fused benzene and α-pyrone rings, for their effects on expression of the type III secretion system (T3SS) of R. solanacearum. Here, we show that umbelliferone (UM), a 7-hydroxycoumarin, suppressed T3SS regulator gene expression through HrpG-HrpB and PrhG-HrpB pathways. UM decreased gene expression of six type III effectors (RipX, RipD, RipP1, RipR, RipTAL, and RipW) of 10 representative effector genes but did not alter T2SS expression. In addition, biofilm formation of R. solanacearum was significantly reduced by UM, though swimming activity was not affected. We then observed that UM suppressed the wilting disease process by reducing colonization and proliferation in tobacco roots and stems. In summary, the findings reveal that UM may serve as a plant-derived inhibitor to manipulate R. solanacearum T3SS and biofilm formation, providing proof of concept that these key virulence factors are potential targets for the integrated control of bacterial wilt.

| S-EPMC5492427 | biostudies-literature

HpaP modulates type III effector secretion in Ralstonia solanacearum and harbours a substrate specificity switch domain essential for virulence.

Project description:Many pathogenic bacteria have evolved a type III secretion system (T3SS) to successfully invade their host. This extracellular apparatus allows the translocation of proteins, called type III effectors (T3Es), directly into the host cells. T3Es are virulence factors that have been shown to interfere with the host's immunity or to provide nutrients from the host to the bacteria. The Gram-negative bacterium Ralstonia solanacearum is a worldwide major crop pest whose virulence strongly relies on the T3SS. In R.?solanacearum, transcriptional regulation has been extensively studied. However, very few data are available concerning the role played by type III-associated regulators, such as type III chaperones and T3SS control proteins. Here, we characterized HpaP, a putative type III secretion substrate specificity switch (T3S4) protein of R.?solanacearum which is not secreted by the bacterium or translocated in the plant cells. HpaP self-interacts and interacts with the PopP1 T3E. HpaP modulates the secretion of early (HrpY pilin) and late (AvrA and PopP1 T3Es) type III substrates. HpaP is dispensable for the translocation of T3Es into the host cells. Finally, we identified two regions of five amino acids in the T3S4 domain that are essential for efficient PopP1 secretion and for HpaP's role in virulence on tomato and Arabidopsis thaliana, but not required for HpaP-HpaP and HpaP-PopP1 interactions. Taken together, our results indicate that HpaP is a putative R.?solanacearum?T3S4 protein important for full pathogenicity on several hosts, acting as a helper for PopP1 secretion, and repressing AvrA and HrpY secretion.

| S-EPMC6638691 | biostudies-literature

ClpV3 of the H3-Type VI Secretion System (H3-T6SS) Affects Multiple Virulence Factors in Pseudomonas aeruginosa.

Project description:The type VI secretion system (T6SS) is a toxic effector delivery apparatus widely distributed in Gram-negative bacteria. The opportunistic pathogen Pseudomonas aeruginosa encodes three T6SSs, namely H1-, H2-, and H3-T6SS. Each T6SS possesses its own effectors and their roles are not yet fully understood. Here, we report that an H3-T6SS deletion mutant PAO1(?clpV3) significantly affected the virulence-related phenotypes including pyocyanin production, biofilm formation, proteolytic activity, and motilities. Most interestingly, the expression of T3SS genes was markedly affected, indicating a link between H3-T6SS and T3SS. RNA-Sequencing was performed to globally identify the genes differentially expressed when H3-T6SS was inactivated and the results obtained correlated well with the observed phenotypes. Interestingly, the expressions of T2SS, T3SS, H2-T6SS, and H3-T6SS were all significantly decreased, while H1-T6SS was increased in the PAO1(?clpV3) strain. We also observed that the intracellular concentration of secondary messenger cAMP was reduced in PAO1(?clpV3), and the c-di-GMP level was also decreased as indicated by the decreased cdrA reporter activity. Finally, by using a Galleria mellonella infection model, we show that H3-T6SS plays a key role in the pathogenicity of P. aeruginosa in vivo. Overall, our study highlights the unique connection of H3-T6SS in P. aeruginosa with T3SS, pyocyanin production, biofilm formation and in vivo pathogenicity.

| S-EPMC7273116 | biostudies-literature

Ralstonia solanacearum type III secretion system effector Rip36 induces a hypersensitive response in the nonhost wild eggplant Solanum torvum.

Project description:Ralstonia solanacearum is a Gram-negative soil-borne bacterium that causes bacterial wilt disease in more than 200 plant species, including economically important Solanaceae species. In R. solanacearum, the hypersensitive response and pathogenicity (Hrp) type III secretion system is required for both the ability to induce the hypersensitive response (HR) in nonhost plants and pathogenicity in host plants. Recently, 72 effector genes, called rip (Ralstonia protein injected into plant cells), have been identified in R. solanacearum RS1000. RS1002, a spontaneous nalixidic acid-resistant derivative of RS1000, induced strong HR in the nonhost wild eggplant Solanum torvum in an Hrp-dependent manner. An Agrobacterium-mediated transient expression system revealed that Rip36, a putative Zn-dependent protease effector of R. solanacearum, induced HR in S. torvum. A mutation in the putative Zn-binding motif (E149A) completely abolished the ability to induce HR. In agreement with this result, the RS1002-derived Δrip36 and rip36E149A mutants lost the ability to induce HR in S. torvum. An E149A mutation had no effect on the translocation of Rip36 into plant cells. These results indicate that Rip36 is an avirulent factor that induces HR in S. torvum and that a putative Zn-dependent protease motif is essential for this activity.

| S-EPMC6638889 | biostudies-other

Involvement of ralfuranones in the quorum sensing signalling pathway and virulence of Ralstonia solanacearum strain OE1-1.

Project description:The soil-borne, plant-pathogenic Ralstonia solanacearum strain OE1-1 produces and secretes methyl 3-hydroxymyristate (3-OH MAME) as a quorum sensing (QS) signal, which contributes to its virulence. A global virulence regulator, PhcA, functioning through the QS system, positively regulates the expression of ralA, which encodes furanone synthase, to produce aryl-furanone secondary metabolites, ralfuranones. A ralfuranone-deficient mutant (ΔralA) is weakly virulent when directly inoculated into tomato xylem vessels. To investigate the functions of ralfuranones, we analysed R. solanacearum transcriptome data generated by RNA sequencing technology. ΔralA expressed phcB, which is associated with 3-OH MAME production, and phcA at levels similar to those in strain OE1-1. In addition, ΔralA exhibited down-regulated expression of more than 90% of the QS positively regulated genes, and up-regulated expression of more than 75% of the QS negatively regulated genes. These results suggest that ralfuranones affect the QS feedback loop. Ralfuranone supplementation restored the ability of ΔralA cells to aggregate. In addition, ralfuranones A and B restored the swimming motility of ΔralA to wild-type levels. However, the application of exogenous ralfuranones did not affect the production of the major exopolysaccharide, EPS I, in ΔralA. Quantitative real-time polymerase chain reaction assays revealed that the deletion of ralA results in the down-regulated expression of vsrAD and vsrBC, which encode a sensor kinase and a response regulator, respectively, in the two-component regulatory systems that influence EPS I production. The application of ralfuranone B restored the expression of these two genes. Overall, our findings indicate that integrated signalling via ralfuranones influences the QS and virulence of R. solanacearum.

| S-EPMC6638173 | biostudies-literature

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