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Structural Profiling of Bioactive Compounds with Medicinal Potential from Traditional Indian Medicinal Plants
Published in Jayanta Kumar Patra, Gitishree Das, Sanjeet Kumar, Hrudayanath Thatoi, Ethnopharmacology and Biodiversity of Medicinal Plants, 2019
C. Sareena, A. Anju Suresh, Swetha Sunil, T. V. Suchithra
The killing effect of benzoic acid on Burkholderia xenovorans has been studied, and several targets were reported such as amidase, putative carbon-nitrogen hydrolase protein, 2-hydroxy-6-oxo-6-phenylhexa-2, 4-dienoate hydrolase (BphD), benzoate 1, 2-dioxygenase (BenA, BenB, and BenC), benzaldehyde dehydrogenase and benzoate-coenzyme A ligase. While amidase and putative carbon-nitrogen hydrolase protein affect virulence factor, others can block drug metabolism (Stitch 4.0.). Another virulence factor such as AmtR, a transcriptional regulator that present in Corynebacterium glutamicum can be inhibited by p-cymene. Kovac et al., studied the target action of α-pinene in Campylobacter jejuni and found it can bind to HrcA and HspR which are efflux pump proteins of the bacteria (Kovac et al., 2015). The most studied phytocompounds against E. coli are berberine, chlorogenic acid, cinnamaldehyde, EGCG, quercetin diacylglycoside, thymoquinone, curcumin, linoleic acid, and sabinene. Among them, curcumin, EGCG and quercetin diacylglycoside possess multiple targets in E. coli. The targets of curcumin are dihydropteridine reductase, FtsZ, predicted NADP-dependent, Zn-dependent oxidoreductase and tyrosine kinase which can block synthesis of nucleotides and amino acids, bacterial division, drug metabolism, extracellular polysaccharide, and colanic acid synthesis respectively (Stitch 4.0.). While EGCG has only two targets-Fab G and Fab I which function in fatty acid biosynthesis (Zhang and Rock, 2004). Like EGCG, linoleic acid also can target on Fab I. Quercetin diacylglycoside targets on DNA gyrase B (Suriyanarayanan et al., 2013) and topoisomerase IV (Hossion et al., 2011) which are responsible for negative supercoiling of DNA and resolution of chromosome dimers at DNA replication. Sabinene inhibits the adhesion of E. Coli to host cells by binding to YfcC, a predicted membrane protein.
Biosynthesis and Genetics of Lipopolysaccharide Core
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
David E. Heinrichs, Chris Whitfield, Miguel A. Valvano
Mutants with defects in the backbone heptose residues are stable under laboratory conditions but give rise to the pleiotropic phenotype known as “deep-rough.” However, the precise involvement of heptosyl residues in the deep-rough phenotype is obscured because these residues provide the site of modification by phosphoryl groups and phosphoryl derivatives (Fig. 2). The deep-rough phenotype has been discussed at length in a number of recent reviews (4,10,19,147), and we refer the reader to these reviews for a more detailed description and pertinent references. Briefly, deep-rough LPS mutants characteristically have changes in surface hydrophilicity, resulting in hypersensitivity to hydrophobic dyes, detergents, hydrophobic antibiotics, fatty acids, phenols, and polycyclic hydrocarbons. The wild-type outer membrane normally has limited permeability to these compounds, and they are toxic only in high concentrations. The increased outer membrane permeability of these mutants appears to reflect major compositional and structural changes in the outer membrane, resulting from the defect in LPS biosynthesis. LPS interacts with divalent cations that help maintain the structural integrity of the outer membrane. Mutants with deep-rough LPS typically release significant amounts of periplasmic enzymes into the culture media. The outer membrane is stabilized by growth in media supplemented with high concentrations of Mg2+, and the release of enzymes is reduced. The outer membrane of some deep-rough mutants has also been reported to have a decreased protein content with a concomitant increase in phospholipid. The reduction in protein content may be a consequence of reduced trimerization of porin monomers. The compromised outer membrane integrity of the deep-rough LPS mutants increases their susceptibility to attack by lysosomal fractions of polymorphonuclear leukocytes and phagocytosis by macrophages (20). In addition to the above observations, deep-rough mutants of E. coli K-12 are associated with increased expression of colanic acid capsular polysaccharide (21) and the loss of pili and flagella in deep-rough mutants of E. coli K-12 and Salmonella (21,22). It is possible that these latter pheno-types are a general response to outer membrane perturbation.
Outer membrane vesicles induce the mussel plantigrade settlement via regulation of c-di-GMP
Published in Biofouling, 2023
Guanju Wu, Xiao-Meng Hu, Li-Hua Peng, Wen Zhang, Xiao Liang, Sergey Dobretsov, Jin-Long Yang
The present work provides evidence that altering c-di-GMP levels in tolB mutant resulted in a reduction of mussel settlement. The present study has demonstrated that bacterial c-di-GMP influences the mussel settlement by regulating colanic acid content (Peng et al. 2020). The biofilms formed by the deletion of the cellulose biosynthesis gene bcsQ in P. marina inhibited mussel larval settlement, and the further study demonstrated the regulation of the bcsQ gene is mediated by altering c-di-GMP level to affect biofilms formation and EPS (Liang et al. 2021). The deletion of the bacterial thioesterase gene tesA contributed to an increase in c-di-GMP content and a reduced fatty acid secretion, which inhibited larval settlement (Hu et al. 2021). Thus, c-di-GMP plays a crucial role in regulating mussel settlement by altering biofilm formation and secretion of EPS, including extracellular polysaccharides, lipids, and OMVs.
Molecules involved in motility regulation in Escherichia coli cells: a review
Published in Biofouling, 2020
Fazlurrahman Khan, Nazia Tabassum, Dung Thuy Nguyen Pham, Sandra Folarin Oloketuyi, Young-Mog Kim
RcsCDB phosphorelay is a signaling system that is found only in Enterobacterales, including E. coli. This system is important for the regulation of capsular polysaccharide colanic acid synthesis, cell division, cell wall maintenance, stationary-phase sigma factor σS, motility, and virulence (Wang et al. 2007). The RcsCDB system has been shown to negatively regulate flagellar activity and virulence by recruiting RcsA and RcsB response regulators, RcsC membrane sensor kinase, and membrane-bound RcsD phosphotransfer protein (Majdalani and Gottesman 2005). Formation of a heterodimer consisting of RcsB and RcsA is required for binding to the flhD promoter, which then allows inhibition of flagellar gene synthesis (Francez-Charlot et al. 2003). The RcsCDB system also downregulates the expression of curli gene csgD in E. coli (Ferrières and Clarke 2003). Apart from the negative regulatory role in the flagella synthesis, the RcsCDB system is also involved in colanic acid synthesis, which contributes to biofilm maturation as an extracellular polymeric substance (Gottesman et al. 1985). RcsB homodimer is also responsible for the positive regulation of transcription of colonic acid synthesis gene wza (Trisler and Gottesman 1984).
Nanotoxicity of engineered nanomaterials (ENMs) to environmentally relevant beneficial soil bacteria – a critical review
Published in Nanotoxicology, 2019
Ricky W. Lewis, Paul M. Bertsch, David H. McNear
Another study investigated the role of EPS in modulating sodium citrate-stabilized Ag ENM (10–100 nm) toxicity by exposing Si. meliloti Rm 1021, Rm 7096 – an EPS overproducing mutant, and Rm 7210 – an EPS lacking mutant in LB medium (Joshi et al. 2012). Consistent with the most literature, EPS over-producing mutants exhibited greater tolerance of Ag ENMs. Particle size was estimated in the medium and dissolution measurements, along with responses to silver ion controls, suggested that abiotic Ag ENM dissolution did not explain the observed responses (which is different than the results of Lewis et al. (2017), where the abiotically dissolved fraction was reported to likely explain the toxicity of PVP-Ag ENMs to Si. meliloti 2011.) E. coli JM109/pEdinbrick1, which produces low levels of colanic acid, was also exposed to 56–76 µM Ag ENMs, and the addition of an EPS analog, xanthan, increased survival by 10–25%. Furthermore, the addition of EPS purified from E. coli JM109/pRscA2 increased survival by 40% in response to 60 µM Ag ENMs in E. coli/BW25113/Δyhak, which produces low levels of polysaccharides.