@article{PAR00011498,
  title = {{A} toxin-antitoxin module of {S}almonella promotes virulence in mice},
  author = {{D}e la {C}ruz, {M}. {A}. and {Z}hao, {W}. {D}. and {F}arenc, {C}. and {G}imenez, {G}. and {R}aoult, {D}idier and {C}ambillau, {C}. and {G}orvel, {J}. {P}. and {M}eresse, {S}.},
  editor = {},
  language = {{ENG}},
  abstract = {{T}oxin-antitoxin ({TA}) modules are widely prevalent in both bacteria and archaea. {O}riginally described as stabilizing elements of plasmids, {TA} modules are also widespread on bacterial chromosomes. {T}hese modules promote bacterial persistence in response to specific environmental stresses. {S}o far, the possibility that {TA} modules could be involved in bacterial virulence has been largely neglected, but recent comparative genomic studies have shown that the presence of {TA} modules is significantly associated with the pathogenicity of bacteria. {U}sing {S}almonella as a model, we investigated whether {TA} modules help bacteria to overcome the stress conditions encountered during colonization, thereby supporting virulence in the host. {B}y bioinformatics analyses, we found that the genome of the pathogenic bacterium {S}almonella {T}yphimurium encodes at least 11 type {II} {TA} modules. {S}everal of these are conserved in other pathogenic strains but absent from non-pathogenic species indicating that certain {TA} modules might play a role in {S}almonella pathogenicity. {W}e show that one {TA} module, hereafter referred to as seh{AB}, plays a transient role in virulence in perorally inoculated mice. {T}he use of a transcriptional reporter demonstrated that bacteria in which seh{AB} is strongly activated are predominantly localized in the mesenteric lymph nodes. {I}n addition, seh{AB} was shown to be important for the survival of {S}almonella in these peripheral lymphoid organs. {T}hese data indicate that the transient activation of a type {II} {TA} module can bring a selective advantage favouring virulence and demonstrate that {TA} modules are engaged in {S}almonella pathogenesis.},
  keywords = {},
  booktitle = {},
  journal = {{P}los {P}athogens},
  volume = {9},
  numero = {12},
  pages = {e1003827},
  ISSN = {1553-7374},
  year = {2013},
  DOI = {10.1371/journal.ppat.1003827},
  URL = {https://www.documentation.ird.fr/hor/{PAR}00011498},
}