A bile-inducible membrane protein mediates bifidobacterial bile resistance

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TY  - JOUR
  - Ruiz, L.,O'Connell-Motherway, M.,Zomer, A.,de los Reyes-Gavilan, C. G.,Margolles, A.,van Sinderen, D.
  - 2012
  - July
  - A bile-inducible membrane protein mediates bifidobacterial bile resistance
  - Validated
  - ()
  - 5
  - 44
  - 523
  - 35523
  - Bbr_0838 from Bifidobacterium breve UCC2003 is predicted to encode a 683 residue membrane protein, containing both a permease domain that displays similarity to transporters belonging to the major facilitator superfamily, as well as a CBS (cystathionine beta synthase) domain. The high level of similarity to bile efflux pumps from other bifidobacteria suggests a significant and general role for Bbr_0838 in bile tolerance. Bbr_0838 transcription was shown to be monocistronic and strongly induced upon exposure to bile. Further analysis delineated the transcriptional start site and the minimal region required for promoter activity and bile regulation. Insertional inactivation of Bbr_0838 in B. breve UCC2003 resulted in a strain, UCC2003:838(800) , which exhibited reduced survival upon cholate exposure as compared with the parent strain, a phenotype that was reversed when a functional, plasmid-encoded Bbr_0838 gene was introduced into UCC2003:838(800) . Transcriptome analysis of UCC2003:838(800) grown in the presence or absence of bile demonstrated that transcription of Bbr_0832, which is predicted to encode a macrolide efflux transporter gene, was significantly increased in the presence of bile, representing a likely compensatory mechanism for bile removal in the absence of Bbr_0838. This study represents the first in-depth analysis of a bile-inducible locus in bifidobacteria, identifying a key gene relevant for bifidobacterial bile tolerance.Bbr_0838 from Bifidobacterium breve UCC2003 is predicted to encode a 683 residue membrane protein, containing both a permease domain that displays similarity to transporters belonging to the major facilitator superfamily, as well as a CBS (cystathionine beta synthase) domain. The high level of similarity to bile efflux pumps from other bifidobacteria suggests a significant and general role for Bbr_0838 in bile tolerance. Bbr_0838 transcription was shown to be monocistronic and strongly induced upon exposure to bile. Further analysis delineated the transcriptional start site and the minimal region required for promoter activity and bile regulation. Insertional inactivation of Bbr_0838 in B. breve UCC2003 resulted in a strain, UCC2003:838(800) , which exhibited reduced survival upon cholate exposure as compared with the parent strain, a phenotype that was reversed when a functional, plasmid-encoded Bbr_0838 gene was introduced into UCC2003:838(800) . Transcriptome analysis of UCC2003:838(800) grown in the presence or absence of bile demonstrated that transcription of Bbr_0832, which is predicted to encode a macrolide efflux transporter gene, was significantly increased in the presence of bile, representing a likely compensatory mechanism for bile removal in the absence of Bbr_0838. This study represents the first in-depth analysis of a bile-inducible locus in bifidobacteria, identifying a key gene relevant for bifidobacterial bile tolerance.
  - 1751-7915 (Electronic) 17
  - http://www.ncbi.nlm.nih.gov/pubmed/22296641http://www.ncbi.nlm.nih.gov/pubmed/22296641
DA  - 2012/07
ER  - 
@article{V191490364,
   = {Ruiz,  L. and O'Connell-Motherway,  M. and Zomer,  A. and de los Reyes-Gavilan,  C. G. and Margolles,  A. and van Sinderen,  D. },
   = {2012},
   = {July},
   = {A bile-inducible membrane protein mediates bifidobacterial bile resistance},
   = {Validated},
   = {()},
   = {5},
   = {44},
  pages = {523--35523},
   = {{Bbr_0838 from Bifidobacterium breve UCC2003 is predicted to encode a 683 residue membrane protein, containing both a permease domain that displays similarity to transporters belonging to the major facilitator superfamily, as well as a CBS (cystathionine beta synthase) domain. The high level of similarity to bile efflux pumps from other bifidobacteria suggests a significant and general role for Bbr_0838 in bile tolerance. Bbr_0838 transcription was shown to be monocistronic and strongly induced upon exposure to bile. Further analysis delineated the transcriptional start site and the minimal region required for promoter activity and bile regulation. Insertional inactivation of Bbr_0838 in B. breve UCC2003 resulted in a strain, UCC2003:838(800) , which exhibited reduced survival upon cholate exposure as compared with the parent strain, a phenotype that was reversed when a functional, plasmid-encoded Bbr_0838 gene was introduced into UCC2003:838(800) . Transcriptome analysis of UCC2003:838(800) grown in the presence or absence of bile demonstrated that transcription of Bbr_0832, which is predicted to encode a macrolide efflux transporter gene, was significantly increased in the presence of bile, representing a likely compensatory mechanism for bile removal in the absence of Bbr_0838. This study represents the first in-depth analysis of a bile-inducible locus in bifidobacteria, identifying a key gene relevant for bifidobacterial bile tolerance.Bbr_0838 from Bifidobacterium breve UCC2003 is predicted to encode a 683 residue membrane protein, containing both a permease domain that displays similarity to transporters belonging to the major facilitator superfamily, as well as a CBS (cystathionine beta synthase) domain. The high level of similarity to bile efflux pumps from other bifidobacteria suggests a significant and general role for Bbr_0838 in bile tolerance. Bbr_0838 transcription was shown to be monocistronic and strongly induced upon exposure to bile. Further analysis delineated the transcriptional start site and the minimal region required for promoter activity and bile regulation. Insertional inactivation of Bbr_0838 in B. breve UCC2003 resulted in a strain, UCC2003:838(800) , which exhibited reduced survival upon cholate exposure as compared with the parent strain, a phenotype that was reversed when a functional, plasmid-encoded Bbr_0838 gene was introduced into UCC2003:838(800) . Transcriptome analysis of UCC2003:838(800) grown in the presence or absence of bile demonstrated that transcription of Bbr_0832, which is predicted to encode a macrolide efflux transporter gene, was significantly increased in the presence of bile, representing a likely compensatory mechanism for bile removal in the absence of Bbr_0838. This study represents the first in-depth analysis of a bile-inducible locus in bifidobacteria, identifying a key gene relevant for bifidobacterial bile tolerance.}},
  issn = {1751-7915 (Electronic) 17},
   = {http://www.ncbi.nlm.nih.gov/pubmed/22296641http://www.ncbi.nlm.nih.gov/pubmed/22296641},
  source = {IRIS}
}
AUTHORSRuiz, L.,O'Connell-Motherway, M.,Zomer, A.,de los Reyes-Gavilan, C. G.,Margolles, A.,van Sinderen, D.
YEAR2012
MONTHJuly
JOURNAL_CODE
TITLEA bile-inducible membrane protein mediates bifidobacterial bile resistance
STATUSValidated
TIMES_CITED()
SEARCH_KEYWORD
VOLUME5
ISSUE44
START_PAGE523
END_PAGE35523
ABSTRACTBbr_0838 from Bifidobacterium breve UCC2003 is predicted to encode a 683 residue membrane protein, containing both a permease domain that displays similarity to transporters belonging to the major facilitator superfamily, as well as a CBS (cystathionine beta synthase) domain. The high level of similarity to bile efflux pumps from other bifidobacteria suggests a significant and general role for Bbr_0838 in bile tolerance. Bbr_0838 transcription was shown to be monocistronic and strongly induced upon exposure to bile. Further analysis delineated the transcriptional start site and the minimal region required for promoter activity and bile regulation. Insertional inactivation of Bbr_0838 in B. breve UCC2003 resulted in a strain, UCC2003:838(800) , which exhibited reduced survival upon cholate exposure as compared with the parent strain, a phenotype that was reversed when a functional, plasmid-encoded Bbr_0838 gene was introduced into UCC2003:838(800) . Transcriptome analysis of UCC2003:838(800) grown in the presence or absence of bile demonstrated that transcription of Bbr_0832, which is predicted to encode a macrolide efflux transporter gene, was significantly increased in the presence of bile, representing a likely compensatory mechanism for bile removal in the absence of Bbr_0838. This study represents the first in-depth analysis of a bile-inducible locus in bifidobacteria, identifying a key gene relevant for bifidobacterial bile tolerance.Bbr_0838 from Bifidobacterium breve UCC2003 is predicted to encode a 683 residue membrane protein, containing both a permease domain that displays similarity to transporters belonging to the major facilitator superfamily, as well as a CBS (cystathionine beta synthase) domain. The high level of similarity to bile efflux pumps from other bifidobacteria suggests a significant and general role for Bbr_0838 in bile tolerance. Bbr_0838 transcription was shown to be monocistronic and strongly induced upon exposure to bile. Further analysis delineated the transcriptional start site and the minimal region required for promoter activity and bile regulation. Insertional inactivation of Bbr_0838 in B. breve UCC2003 resulted in a strain, UCC2003:838(800) , which exhibited reduced survival upon cholate exposure as compared with the parent strain, a phenotype that was reversed when a functional, plasmid-encoded Bbr_0838 gene was introduced into UCC2003:838(800) . Transcriptome analysis of UCC2003:838(800) grown in the presence or absence of bile demonstrated that transcription of Bbr_0832, which is predicted to encode a macrolide efflux transporter gene, was significantly increased in the presence of bile, representing a likely compensatory mechanism for bile removal in the absence of Bbr_0838. This study represents the first in-depth analysis of a bile-inducible locus in bifidobacteria, identifying a key gene relevant for bifidobacterial bile tolerance.
PUBLISHER_LOCATION
ISBN_ISSN1751-7915 (Electronic) 17
EDITION
URLhttp://www.ncbi.nlm.nih.gov/pubmed/22296641http://www.ncbi.nlm.nih.gov/pubmed/22296641
DOI_LINK
FUNDING_BODY
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