English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background  Host defence peptides (HDPs), also known as antimicrobial peptides (AMPs), have emerged as potential new therapeutics and their antimicrobial spectrum covers a wide range of target organisms. However, the mode of action and the genetics behind the bacterial response to HDPs is incompletely understood and such knowledge is required to evaluate their potential as antimicrobial therapeutics. Plectasin is a recently discovered HDP active against Gram-positive bacteria with the human pathogen,  Staphylococcus aureus  ( S. aureus ) being highly susceptible and the food borne pathogen,  Listeria monocytogenes  ( L. monocytogenes ) being less sensitive. In the present study we aimed to use transposon mutagenesis to determine the genetic basis for  S. aureus  and  L. monocytogenes  susceptibility to plectasin.    Results  In order to identify genes that provide susceptibility to plectasin we constructed bacterial transposon mutant libraries of  S. aureus  NCTC8325-4 and  L. monocytogenes  4446 and screened for increased resistance to the peptide. No resistant mutants arose when  L. monocytogenes  was screened on plates containing 5 and 10 fold Minimal Inhibitory Concentration (MIC) of plectasin. However, in  S. aureus , four mutants with insertion in the heme response regulator ( hssR ) were 2-4 fold more resistant to plectasin as compared to the wild type. The  hssR  mutation also enhanced resistance to the plectasin-like defensin eurocin, but not to other classes of HDPs or to other stressors tested. Addition of plectasin did not influence the expression of  hssR  or  hrtA , a gene regulated by HssR. The genome of  L. monocytogenes  LO28 encodes a putative HssR homologue, RR23 (in  L. monocytogenes  EGD-e lmo2583) with 48% identity to the  S. aureus  HssR, but a mutation in the  rr23  gene did not change the susceptibility of  L. monocytogenes  to plectasin.    Conclusions   S. aureus  HssR, but not the homologue RR23 from  L. monocytogenes , provides susceptibility to the defensins plectasin and eurocin. Our data suggest that a functional difference between response regulators HssR and RR23 is responsible for the difference in plectasin susceptibility observed between  S. aureus  and  L. monocytogenes .

bmc microbiology

The heme sensing response regulator HssR in Staphylococcus aureus but not the homologous RR23 in Listeria monocytogenes modulates susceptibility to the antimicrobial peptide plectasin