We are very grateful to Sir David Hopwood for critical reading of

We are very grateful to Sir David Hopwood for critical reading of and useful suggestions and corrections on the manuscript. We thank Huarong Tan for kindly providing a cosmid containing the entire nikkomycin biosynthetic gene cluster. This work was supported by grants from National ‘973’ project (2011CBA00801), National Nature Science Foundation of China (31121001), and the Chinese Academy of Sciences project (KSCX2-EW-G-13) to Z.Q. M.Z., X.J., and P.X. contributed equally to this work. Please note: Wiley-Blackwell is not responsible

for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Microbiology, St. Joseph’s click here Health Centre, Toronto, ON, Canada Pseudomonas aeruginosa PA96 is a clinical isolate from Guangzhou, China, that is multiresistant to antibiotics. We previously described the 500-kb IncP-2 plasmid, pOZ176 that encodes many resistance genes including the IMP-9 carbapenemase. BMS-777607 nmr Whole-genome sequencing of PA96 enabled characterization of its genomic islands, virulence factors, and chromosomal resistance genes. We filled gaps using PCR and used optical mapping to confirm the correct contig order. We automatically annotated the core genome and manually annotated the genomic islands.

The genome is 6 444 091 bp and encodes 5853 ORFs. From the whole-genome sequence, we constructed a physical map and constructed Teicoplanin a phylogenetic tree for comparison with sequenced P. aeruginosa strains. Analysis of known core genome virulence factors and resistance genes revealed few differences with other strains, but the major virulence island is closer to that of DK2 than to PA14. PA96 most closely resembles the environmental strain M18, and notably shares a common

serotype, pyoverdin type, flagellar operon, type IV pilin, and several genomic islands with M18. “
“Salmonella enterica serovar Typhimurium is an animal and zoonotic pathogen of worldwide importance. Intestinal colonization, induction of enteritis and systemic translocation by this bacterium requires type III protein secretion. Strategies that target this process have the potential to control infection, pathology and transmission. We defined the global transcriptional response of S. Typhimurium to INP0403, a member of a family of salicylidene acylhydrazides that inhibit type III secretion (T3S). INP0403 treatment was associated with reduced transcription of genes involved in T3S, but also increased transcription of genes associated with iron acquisition. We show that INP0403 restricts iron availability to Salmonella, and that inhibition of T3S system-1 by INP0403 is, at least in part, reversible by exogenous iron and independent of the iron response regulator Fur.

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