Rational design of inhibitors of VirA–VirG two-component signal transduction

Maresh, Justin J.; Zhang, Jin; Tzeng, Yih-Ling; Goodman, Nora A.; Lynn, David G.

doi:10.1016/j.bmcl.2007.04.018

Cited by 10 publications

(7 citation statements)

References 25 publications

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“…The resultant ester was further acylated using acetyl chloride in carbon disulde into methyl 2-acetyl-3,5dimethoxybenzoate (3) with 52% yield. 19 Demethylation of methyl 2-acetyl-3,5-dimethoxybenzoate (3) using BBr 3 in dichloromethane was attempted as per the procedure reported, 20 however, unfortunately only monomethylated product was obtained. Thus, AlCl 3 was used 21 instead of BBr 3 to get the desired demethylated product in good yield.…”

Section: Resultsmentioning

confidence: 99%

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First synthesis of rugosaflavonoid and its derivatives and their activity against breast cancer

Puranik

Srivastava

2017

RSC Adv.

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Section: Resultsmentioning

confidence: 99%

“…The methyl 3,5-dimethoxybenzoate (5 mmol) was mixed with acetyl chloride (25 mmol) and carbon disulde (2 ml) under dry N 2 in ice bath. 19 To this AlCl 3 (15 mmol) was added under vigorous stirring. The reaction was allowed to stir for 15 min.…”

Section: Methodsmentioning

confidence: 99%

First synthesis of rugosaflavonoid and its derivatives and their activity against breast cancer

Puranik

Srivastava

2017

RSC Adv.

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“…Virulence gene expression is induced in both of these strains by dicot explants, and YHL324 s+ is also induced by monocot tissues. However, this hypersensitive strain did not induce tumors in wounded maize plants, suggesting that pathogen incompatibility in monocots may be limited by other intrinsic factors than those responsible for the initial stages of virulence gene induction (Maresh et al, 2006;Maresh et al, 2007). As outlined in Figure 9, wound healing in dicots involves dedifferentiation and proliferation to repair the wound, but monocot cells lose the ability to dedifferentiate very early in FIGURE 8 | Both VirA wt and VirA Y293F Agrobacterium induce crown gall tumors.…”

Section: Discussionmentioning

confidence: 99%

Mapping Reaction-Diffusion Networks at the Plant Wound Site With Pathogens

et al. 2020

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The rich collection of microbes colonizing the plant root making up the rhizosphere function as a multigenomic organ for nutrient distribution. The extent to which its dynamic mutualistic cellular order depends on morphogenic signaling, while likely, remains unknown. We have shown that reaction-diffusion chemical networks constructed with model plant and bacterial metabolites can mimic processes ranging from oxidative burst kinetics to traveling waves and extracellular stationary state reaction-diffusion networks for spatiotemporal ordering of the rhizosphere. Plant parasites and pathogens can be limited by host attachment require dynamic informational networks and continue to provide insight into what controls the rhizosphere. Here we take advantage of Agrobacterium tumefaciens, a plant pathogen with a gated receptor that requires simultaneous perception of two plant metabolites. Genetic manipulations have created receptors allowing each metabolite concentration to be correlated with pathogen behavior. The development of the florescent strains used here provide initial maps of the reactiondiffusion dynamics existing in the rhizosphere, revealing significant differences in the signaling landscape of host and non-host plants before and after wounding, specifically highlighting networks that may inform rhizosphere organization.

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“…We found that HQ17-2 could increase PB susceptibility in the wild-type but not in the rppA and pmrI mutants of P. mirabilis (Table 3), suggesting that HQ17-2 increase PB susceptibility through the RppAPmrI dependent pathway. HQ17-2 shares structural similarity with the published inhibitor of VirAG TCS [43]. Through binding to the VirA sensor, the VirAG inhibitor competes with phenol, which is the inducer of VirAG TCS [43].…”

Section: Discussionmentioning

confidence: 99%

“…HQ17-2 shares structural similarity with the published inhibitor of VirAG TCS [43]. Through binding to the VirA sensor, the VirAG inhibitor competes with phenol, which is the inducer of VirAG TCS [43]. Whether HQ17-2 could act as the RppAB inhibitor by targeting RppB sensor to interfere with autophosphorylation and phosphotransfer to RppA is not known.…”

Section: Discussionmentioning

confidence: 99%

10′(Z),13′(E)-Heptadecadienylhydroquinone Inhibits Swarming and Virulence Factors and Increases Polymyxin B Susceptibility in Proteus mirabilis

et al. 2012

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In this study, we demonstrated that 10′(Z), 13′(E)-heptadecadienylhydroquinone (HQ17-2), isolated from the lacquer tree, could decrease swarming motility and hemolysin activity but increase polymyxin B (PB) susceptibilityof Proteus mirabilis which is intrinsically highly-resistant to PB. The increased PB susceptibility induced by HQ17-2 was also observed in clinical isolates and biofilm-grown cells. HQ17-2 could inhibit swarming in the wild-type and rppA mutant but not in the rcsB mutant, indicating that HQ17-2 inhibits swarming through the RcsB-dependent pathway, a two-component signaling pathway negatively regulating swarming and virulence factor expression. The inhibition of hemolysin activity by HQ17-2 is also mediated through the RcsB-dependent pathway, because HQ17-2 could not inhibit hemolysin activity in the rcsB mutant. Moreover, the finding that HQ17-2 inhibits the expression of flhDC gene in the wild-type and rcsB-complemented strain but not in the rcsB mutant supports the notion. By contrast, HQ17-2 could increase PB susceptibility in the wild-type and rcsB mutant but not in the rppA mutant, indicating that HQ17-2 increases PB susceptibility through the RppA-dependent pathway, a signaling pathway positively regulating PB resistance. In addition, HQ17-2 could inhibit the promoter activities of rppA and pmrI, a gene positively regulated by RppA and involved in PB resistance, in the wild-type but not in the rppA mutant. The inhibition of rppA and pmrI expression caused lipopolysaccharide purified from HQ17-2-treated cells to have higher affinity for PB. Altogether, this study uncovers new biological effects of HQ17-2 and provides evidence for the potential of HQ17-2 in clinical applications.

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Rational design of inhibitors of VirA–VirG two-component signal transduction

Cited by 10 publications

References 25 publications

First synthesis of rugosaflavonoid and its derivatives and their activity against breast cancer

First synthesis of rugosaflavonoid and its derivatives and their activity against breast cancer

Mapping Reaction-Diffusion Networks at the Plant Wound Site With Pathogens

10′(Z),13′(E)-Heptadecadienylhydroquinone Inhibits Swarming and Virulence Factors and Increases Polymyxin B Susceptibility in Proteus mirabilis

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