An H-NS-like Stealth Protein Aids Horizontal DNA Transmission in Bacteria

Abstract

The Sfh protein is encoded by self-transmissible plasmids involved in human typhoid and is closely related to the global regulator H-NS. We have found that Sfh provides a stealth function that allows the plasmids to be transmitted to new bacterial hosts with minimal effects on their fitness. Introducing the plasmid without the sfh gene imposes a mild H-NS(-) phenotype and a severe loss of fitness due to titration of the cellular pool of H-NS by the A+T-rich plasmid. This stealth strategy seems to be used widely to aid horizontal DNA transmission and has important implications for bacterial evolution.

Anti-silencing: overcoming H-NS-mediated repression of transcription in Gram-negative enteric bacteria

“…There is no evidence that StpA interferes with or enhances the ability of H-NS to repress transcription and so the biological role of StpA-H-NS heterodimers remains obscure. So too does the significance of the Sfh-H-NS heteromer, in which H-NS interacts with the Sfh protein, a plasmid-encoded full-length H-NS orthologue Deighan et al, 2003;Doyle & Dorman, 2006;Doyle et al, 2007). A study carried out in uropathogenic E. coli using microarray analysis suggests that H-NS-H-NS homodimers and H-NS-StpA heterodimers may control distinct regulons (Müller et al, 2006).…”

The influence of the accessory genome on bacterial pathogen evolution

“…25 This plasmid has a 55% A + T content and titrates the cell global transcriptional repressor protein H-NS, which binds to A + T-rich sequences. 25,26 This would normally cause a significant reduction in bacterial fitness, but this is avoided by the plasmid-encoded gene sfh, which is a paralogue of H-NS. Sfh binds to most of the H-NS targets in the chromosome, thus allowing pSf-R27 transfer with a minimal impact to the cell.…”

Emergence of plasmid-mediated multidrug resistance in epidemic and non-epidemic strains of Salmonella enterica serotype Typhi from Jordan

“…The presence of strains harboring the IncHI1 plasmid after the outbreak is of concern and poses the problem of it continuing to spread [32] and transfer resistance. Besides plasmids, mobile elements contribute to the dissemination of antibiotic resistance and integrons represent the major vehicle for spread [33].…”