scholarly journals Genetic Interference Analysis Reveals that Both 3-Hydroxybenzoic Acid and 4-Hydroxybenzoic Acid Are Involved in Xanthomonadin Biosynthesis in the Phytopathogen Xanthomonas campestris pv. campestris

2020 ◽  
Vol 110 (2) ◽  
pp. 278-286
Author(s):  
Xue-Qiang Cao ◽  
Xing-Yu Ouyang ◽  
Bo Chen ◽  
Kai Song ◽  
Lian Zhou ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Virulence Factor ◽  
Xanthomonas Campestris ◽  
Gene Clusters ◽  
Hydroxybenzoic Acid ◽  
Factor Production ◽  
In The Wild ◽  
Genetic Interference ◽  
Xanthomonas Campestris Pv Campestris ◽  
Virulence Factor Production

A characteristic feature of phytopathogenic Xanthomonas bacteria is the production of yellow membrane-bound pigments called xanthomonadins. Previous studies showed that 3-hydroxybenzoic acid (3-HBA) was a xanthomonadin biosynthetic intermediate and also, that it had a signaling role. The question of whether the structural isomers 4-HBA and 2-HBA (salicylic acid) have any role in xanthomonadin biosynthesis remained unclear. In this study, we have selectively eliminated 3-HBA, 4-HBA, or the production of both by expression of the mhb, pobA, and pchAB gene clusters in the Xanthomonas campestris pv. campestris strain XC1. The resulting strains were different in pigmentation, virulence factor production, and virulence. These results suggest that both 3-HBA and 4-HBA are involved in xanthomonadin biosynthesis. When both 3-HBA and 4-HBA are present, X. campestris pv. campestris prefers 3-HBA for Xanthomonadin-A biosynthesis; the 3-HBA–derived Xanthomonadin-A was predominant over the 4-HBA–derived xanthomonadin in the wild-type strain XC1. If 3-HBA is not present, then 4-HBA is used for biosynthesis of a structurally uncharacterized Xanthomonadin-B. Salicylic acid had no effect on xanthomonadin biosynthesis. Interference with 3-HBA and 4-HBA biosynthesis also affected X. campestris pv. campestris virulence factor production and reduced virulence in cabbage and Chinese radish. These findings add to our understanding of xanthomonadin biosynthetic mechanisms and further help to elucidate the biological roles of xanthomonadins in X. campestris pv. campestris adaptation and virulence in host plants.

scholarly journals The Host Plant Metabolite Glucose Is the Precursor of Diffusible Signal Factor (DSF) Family Signals in Xanthomonas campestris

2015 ◽  
Vol 81 (8) ◽  
pp. 2861-2868 ◽  
Author(s):  
Yinyue Deng ◽  
Xiaoling Liu ◽  
Ji'en Wu ◽  
Jasmine Lee ◽  
Shaohua Chen ◽  
...  
Keyword(s):  
Host Plant ◽  
Virulence Factor ◽  
Xanthomonas Campestris ◽  
Ethanol Extract ◽  
Burkholderia Cenocepacia ◽  
Content Type ◽  
Communication Signal ◽  
Factor Production ◽  
Diffusible Signal Factor ◽  
Virulence Factor Production

ABSTRACTPlant pathogenXanthomonas campestrispv. campestris producescis-11-methyl-2-dodecenoic acid (diffusible signal factor [DSF]) as a cell-cell communication signal to regulate biofilm dispersal and virulence factor production. Previous studies have demonstrated that DSF biosynthesis is dependent on the presence of RpfF, an enoyl-coenzyme A (CoA) hydratase, but the DSF synthetic mechanism and the influence of the host plant on DSF biosynthesis are still not clear. We show here that exogenous addition of host plant juice or ethanol extract to the growth medium ofX. campestrispv. campestris could significantly boost DSF family signal production. It was subsequently revealed thatX. campestrispv. campestris produces not only DSF but also BDSF (cis-2-dodecenoic acid) and another novel DSF family signal, which was designated DSF-II. BDSF was originally identified inBurkholderia cenocepaciato be involved in regulation of motility, biofilm formation, and virulence inB. cenocepacia. Functional analysis suggested that DSF-II plays a role equal to that of DSF in regulation of biofilm dispersion and virulence factor production inX. campestrispv. campestris. Furthermore, chromatographic separation led to identification of glucose as a specific molecule stimulating DSF family signal biosynthesis inX. campestrispv. campestris.13C-labeling experiments demonstrated that glucose acts as a substrate to provide a carbon element for DSF biosynthesis. The results of this study indicate thatX. campestrispv. campestris could utilize a common metabolite of the host plant to enhance DSF family signal synthesis and therefore promote virulence.

scholarly journals Fatty Acids Regulate Stress Resistance and Virulence Factor Production for Listeria monocytogenes

2012 ◽  
Vol 194 (19) ◽  
pp. 5274-5284 ◽  
Author(s):  
Y. Sun ◽  
B. J. Wilkinson ◽  
T. J. Standiford ◽  
H. T. Akinbi ◽  
M. X. D. O'Riordan
Keyword(s):  
Fatty Acids ◽  
Listeria Monocytogenes ◽  
Virulence Factor ◽  
Stress Resistance ◽  
Factor Production ◽  
Virulence Factor Production

scholarly journals Cyclo(valine–valine) inhibits Vibrio cholerae virulence gene expression

Microbiology ◽  
2014 ◽  
Vol 160 (6) ◽  
pp. 1054-1062 ◽  
Author(s):  
Amit Vikram ◽  
Vanessa M. Ante ◽  
X. Renee Bina ◽  
Qin Zhu ◽  
Xinyu Liu ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Virulence Factor ◽  
Inhibitory Activity ◽  
Virulence Gene ◽  
Side Chains ◽  
Cyclic Dipeptides ◽  
Virulence Gene Expression ◽  
Factor Production ◽  
Virulence Regulator ◽  
Virulence Factor Production

Vibrio cholerae has been shown to produce a cyclic dipeptide, cyclo(phenylalanine–proline) (cFP), that functions to repress virulence factor production. The objective of this study was to determine if heterologous cyclic dipeptides could repress V. cholerae virulence factor production. To that end, three synthetic cyclic dipeptides that differed in their side chains from cFP were assayed for virulence inhibitory activity in V. cholerae. The results revealed that cyclo(valine–valine) (cVV) inhibited virulence factor production by a ToxR-dependent process that resulted in the repression of the virulence regulator aphA. cVV-dependent repression of aphA was found to be independent of known aphA regulatory genes. The results demonstrated that V. cholerae was able to respond to exogenous cyclic dipeptides and implicated the hydrophobic amino acid side chains on both arms of the cyclo dipeptide scaffold as structural requirements for inhibitory activity. The results further suggest that cyclic dipeptides have potential as therapeutics for cholera treatment.

Impact ofd-amino acid dehydrogenase on virulence factor production by aPseudomonas aeruginosa

2013 ◽  
Vol 59 (9) ◽  
pp. 598-603 ◽  
Author(s):  
Kathryn E. Oliver ◽  
Laura Silo-Suh
Keyword(s):  
Amino Acid ◽  
Virulence Factor ◽  
Bacterial Pathogen ◽  
Optimal Production ◽  
Acid Dehydrogenase ◽  
Amino Acid Dehydrogenase ◽  
Factor Production ◽  
Lung Dysfunction ◽  
Production Of Hydrogen ◽  
Virulence Factor Production

Chronic Pseudomonas aeruginosa infections remain the leading cause of lung dysfunction and mortality for cystic fibrosis (CF) patients. Many other bacteria inhabit the CF lung, but P. aeruginosa utilizes novel strategies that allow it to colonize this environment as the predominant bacterial pathogen. d-Amino acid dehydrogenase encoded by dadA is highly expressed by P. aeruginosa within the CF lung, and it is required for optimal production of hydrogen cyanide by some CF-adapted isolates. To better understand the increased significance of d-amino acid dehydrogenase in P. aeruginosa physiology, we characterized the contribution of the dad operon to virulence factor production. In this study, we determined that DadA is required for optimal production of pyocyanin, pyoverdine, and rhamnolipid by CF-adapted and non-CF-adapted isolates of P. aeruginosa. In addition, DadA is required for optimal production of alginate, biofilm formation, and virulence of a CF-adapted isolated of P. aeruginosa in an alfalfa seedling model of infection. Taken together, the results indicate that DadA plays a pleiotropic role in the production of important virulence factors by P. aeruginosa.

scholarly journals The Vibrio cholerae RND efflux systems impact virulence factor production and adaptive responses via periplasmic sensor proteins

2018 ◽  
Vol 14 (1) ◽  
pp. e1006804 ◽  
Author(s):  
X. Renee Bina ◽  
Mondraya F. Howard ◽  
Dawn L. Taylor-Mulneix ◽  
Vanessa M. Ante ◽  
Dillon E. Kunkle ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Virulence Factor ◽  
Adaptive Responses ◽  
Factor Production ◽  
Sensor Proteins ◽  
Virulence Factor Production

scholarly journals Total Synthesis of Xanthoangelol B and Its Various Fragments: Toward Inhibition of Virulence Factor Production of Staphylococcus aureus

2018 ◽  
Vol 61 (23) ◽  
pp. 10473-10487 ◽  
Author(s):  
Pushpak Mizar ◽  
Rekha Arya ◽  
Truc Kim ◽  
Soyoung Cha ◽  
Kyoung-Seok Ryu ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Total Synthesis ◽  
Virulence Factor ◽  
Factor Production ◽  
Virulence Factor Production

scholarly journals Indole Inhibits ToxR Regulon Expression inVibrio cholerae

2019 ◽  
Vol 87 (3) ◽  
Author(s):  
Mondraya F. Howard ◽  
X. Renee Bina ◽  
James E. Bina
Keyword(s):  
Virulence Factor ◽  
Virulence Gene ◽  
Dependent Manner ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Type Vi Secretion ◽  
Biofilm Production ◽  
Factor Production ◽  
Periplasmic Domain ◽  
Virulence Factor Production

ABSTRACTIndole is a degradation product of tryptophan that functions as a signaling molecule in many bacteria. This includesVibrio cholerae, where indole was shown to regulate biofilm and type VI secretion in nontoxigenic environmental isolates. Indole is also produced by toxigenicV. choleraestrains in the human intestine, but its significance in the host is unknown. We investigated the effects of indole on toxigenicV. choleraeO1 El Tor during growth under virulence inducing conditions. The indole transcriptome was defined by RNA sequencing and showed widespread changes in the expression of genes involved in metabolism, biofilm production, and virulence factor production. In contrast, genes involved in type VI secretion were not affected by indole. We subsequently found that indole repressed genes involved inV. choleraepathogenesis, including the ToxR virulence regulon. Consistent with this, indole inhibited cholera toxin and toxin-coregulated pilus production in a dose-dependent manner. The effects of indole on virulence factor production and biofilm were linked to ToxR and the ToxR-dependent regulator LeuO. The expression ofleuOwas increased by exogenous indole and linked to repression of the ToxR virulence regulon. This process was dependent on the ToxR periplasmic domain, suggesting that indole was a ToxR agonist. This conclusion was further supported by results showing that the ToxR periplasmic domain contributed to indole-mediated increased biofilm production. Collectively, our results suggest that indole may be a niche-specific cue that can function as a ToxR agonist to modulate virulence gene expression and biofilm production inV. cholerae.

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