World Library  


Add to Book Shelf
Flag as Inappropriate
Email this Book

Plos One : Isolation of Salmonella Mutants Resistant to the Inhibitory Effect of Salicylidene Acylhydrazides on Flagella-mediated Motility, Volume 8

By Hensel, Michael

Click here to view

Book Id: WPLBN0003951114
Format Type: PDF eBook :
File Size:
Reproduction Date: 2015

Title: Plos One : Isolation of Salmonella Mutants Resistant to the Inhibitory Effect of Salicylidene Acylhydrazides on Flagella-mediated Motility, Volume 8  
Author: Hensel, Michael
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection
Historic
Publication Date:
Publisher: Plos

Citation

APA MLA Chicago

Hensel, M. (n.d.). Plos One : Isolation of Salmonella Mutants Resistant to the Inhibitory Effect of Salicylidene Acylhydrazides on Flagella-mediated Motility, Volume 8. Retrieved from http://members.worldlibrary.net/


Description
Description : Salicylidene acylhydrazides identified as inhibitors of virulence-mediating type III secretion systems (T3SSs) potentially target their inner membrane export apparatus. They also lead to inhibition of flagellar T3SS-mediated swimming motility in Salmonella enterica serovar. Typhimurium. We show that INP0404 and INP0405 act by reducing the number of flagella/cell. These molecules still inhibit motility of a Salmonella DfliH-fliI-fliJ/flhB(P28T) strain, which lacks three soluble components of the flagellar T3S apparatus, suggesting that they are not the target of this drug family. We implemented a genetic screen to search for the inhibitors’ molecular target(s) using motility assays in the DfliH-fliI/flhB(P28T) background. Both mutants identified were more motile than the background strain in the absence of the drugs, although HM18 was considerably more so. HM18 was more motile than its parent strain in the presence of both drugs while DI15 was only insensitive to INP0405. HM18 was hypermotile due to hyperflagellation, whereas DI15 was not hyperflagellated. HM18 was also resistant to a growth defect induced by high concentrations of the drugs. Whole-genome resequencing of HM18 indicated two alterations within protein coding regions, including one within atpB, which encodes the inner membrane a-subunit of the FOF1-ATP synthase. Reverse genetics indicated that the alteration in atpB was responsible for all of HM18’s phenotypes. Genome sequencing of DI15 uncovered a single A562P mutation within a gene encoding the flagellar inner membrane protein FlhA, the direct role of which in mediating drug insensitivity could not be confirmed. We discuss the implications of these findings in terms of T3SS export apparatus function and drug target identification

 

Click To View

Additional Books


  • Plos One : Kidney Injury Molecule-1 is U... (by )
  • Plos One : Inverted Expression Profiles ... (by )
  • Plos One : Molecular Basis for the Disso... (by )
  • Plos One : Diel Variability in Seawater ... (by )
  • Plos One : Improvement of the Management... (by )
  • Plos One : Organic Solvents as Risk Fact... (by )
  • Plos One : Decision-making Under Risk of... (by )
  • Plos One : High Mannose-binding Antivira... (by )
  • Plos One : Association Between the Prese... (by )
  • Plos One : an Alu-based Phylogeny of Lem... (by )
  • Plos One : Human Bat Possesses Molecular... (by )
  • Plos One : Deletion of Fibroblast Growth... (by )
Scroll Left
Scroll Right

 



Copyright © World Library Foundation. All rights reserved. eBooks from World Library are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.