Control of the <i>Ralstonia solanacearum</i> Type III secretion system (Hrp) genes by the global virulence regulator PhcA

Genin, Stéphane; Brito, Belén; Denny, Timothy P.; Boucher, Christian

doi:10.1016/j.febslet.2005.02.058

Cited by 85 publications

(85 citation statements)

References 26 publications

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“…Mutant strains carrying disruptions of the global virulence regulator phcA (GMI1610; Genin et al, 2005) and the T2SS (gspD gspN deletion mutant strain GRS465) were also used. GMI1559 is a GMI1000 derivative carrying a constitutively expressed GUS (uidA) fusion, and GMI1560 is a hrcV mutant also carrying this uidA reporter fusion (Vailleau et al, 2007).…”

Section: Bacterial Strains and Culture Conditionsmentioning

confidence: 99%

Dissection of Bacterial Wilt on Medicago truncatula Revealed Two Type III Secretion System Effectors Acting on Root Infection Process and Disease Development

et al. 2009

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Ralstonia solanacearum is the causal agent of the devastating bacterial wilt disease, which colonizes susceptible Medicago truncatula via the intact root tip. Infection involves four steps: appearance of root tip symptoms, root tip cortical cell invasion, vessel colonization, and foliar wilting. We examined this pathosystem by in vitro inoculation of intact roots of susceptible or resistant M. truncatula with the pathogenic strain GMI1000. The infection process was type III secretion system dependent and required two type III effectors, Gala7 and AvrA, which were shown to be involved at different stages of infection. Both effectors were involved in development of root tip symptoms, and Gala7 was the main determinant for bacterial invasion of cortical cells. Vessel invasion depended on the host genetic background and was never observed in the resistant line. The invasion of the root tip vasculature in the susceptible line caused foliar wilting. The avrA mutant showed reduced aggressiveness in all steps of the infection process, suggesting a global role in R. solanacearum pathogenicity. The roles of these two effectors in subsequent stages were studied using an assay that bypassed the penetration step; with this assay, the avrA mutant showed no effect compared with the GMI1000 strain, indicating that AvrA is important in early stages of infection. However, later disease symptoms were reduced in the gala7 mutant, indicating a key role in later stages of infection.

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Section: Bacterial Strains and Culture Conditionsmentioning

confidence: 99%

Dissection of Bacterial Wilt on Medicago truncatula Revealed Two Type III Secretion System Effectors Acting on Root Infection Process and Disease Development

et al. 2009

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“…Synthesis of ␤-1,4-endoglucanase and pectin methylesterase are positively regulated at high cell densities (27), while synthesis of endopolygalacturonase, a siderophore, and motility by flagella or type IV pili are negatively regulated (1,5,9,26). The expression of the hrp regulon is also negatively regulated by PhcA at high cell densities (13). Therefore, R. solanacearum has two cell density-dependent phenotypes which are regulated by PhcA, and virulence gene expression controlled by PhcA plays a critical role in successful host plant infection (22).…”

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confidence: 90%

The Global Virulence Regulator PhcA Negatively Controls the Ralstonia solanacearum hrp Regulatory Cascade by Repressing Expression of the PrhIR Signaling Proteins

Yoshimochi¹,

Hikichi²,

Kiba³

et al. 2009

J Bacteriol

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“…Acinetobacter, Brucella, Hafnia, Pantoea, Ralstonia, and Rhodobacter, are reported to possess single QSS which are regulated by AHLs signals of varying acyl chain lengths ( Table 3) [127][128][129][130][131][132][133][134]. The presence of QS has been scarcely reported in extremophiles: (1) AHL based QS in haloalkaliphiles-Natronococcus occultus [135] and Halomonas [136,137], (2) peptide-based QS in hyperthermophileThermotoga maritima [138], and (3) a QSS regulated by furanosyl-borate diester signals in archaea [139].…”

Section: Othersmentioning

confidence: 99%

Potential Emergence of Multi-quorum Sensing Inhibitor Resistant (MQSIR) Bacteria

et al. 2015

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Expression of certain bacterial genes only at a high bacterial cell density is termed as quorum-sensing (QS). Here bacteria use signaling molecules to communicate among themselves. QS mediated genes are generally involved in the expression of phenotypes such as bioluminescence, biofilm formation, competence, nodulation, and virulence. QS systems (QSS) vary from a single in Vibrio spp. to multiple in Pseudomonas and Sinorhizobium species. The complexity of QSS is further enhanced by the multiplicity of signals: (1) peptides, (2) acyl-homoserine lactones, (3) diketopiperazines. To counteract this pathogenic behaviour, a wide range of bioactive molecules acting as QS inhibitors (QSIs) have been elucidated. Unlike antibiotics, QSIs don't kill bacteria and act at much lower concentration than those of antibiotics. Bacterial ability to evolve resistance against multiple drugs has cautioned researchers to develop QSIs which may not generate undue pressure on bacteria to develop resistance against them. In this paper, we have discussed the implications of the diversity and multiplicity of QSS, in acting as an arsenal to withstand attack from QSIs and may use these as reservoirs to develop multi-QSI resistance.

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Control of the Ralstonia solanacearum Type III secretion system (Hrp) genes by the global virulence regulator PhcA

Cited by 85 publications

References 26 publications

Dissection of Bacterial Wilt on Medicago truncatula Revealed Two Type III Secretion System Effectors Acting on Root Infection Process and Disease Development

Dissection of Bacterial Wilt on Medicago truncatula Revealed Two Type III Secretion System Effectors Acting on Root Infection Process and Disease Development

The Global Virulence Regulator PhcA Negatively Controls the Ralstonia solanacearum hrp Regulatory Cascade by Repressing Expression of the PrhIR Signaling Proteins

Potential Emergence of Multi-quorum Sensing Inhibitor Resistant (MQSIR) Bacteria

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