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المؤلفStenson, Trevor H.
المؤلفAllen, Andrew G.
المؤلفAl-Meer, Jehan A.
المؤلفMaskell, Duncan, 1961-
المؤلفPeppler, Mark S.
تاريخ الإتاحة2009-12-28T15:20:20Z
تاريخ النشر2005-09
اسم المنشورInfection and Immunity
الاقتباسInfection and Immunity, September 2005, p. 5995-6004, Vol. 73, No. 9
الرقم المعياري الدولي للكتاب0019-9567
معرّف المصادر الموحدhttp://dx.doi.org/10.1128/IAI.73.9.5995-6004.2005
معرّف المصادر الموحدhttp://hdl.handle.net/10576/10538
الملخصExpression of virulence determinants by Bordetella pertussis, the primary etiological agent of whooping cough, is regulated by the BvgAS two-component regulatory system. The role of a second two-component regulatory system, encoded by risAS, in this process is not defined. Here, we show that mutation of B. pertussis risA does not affect Bvg-activated genes or proteins. However, mutation of risA resulted in greatly diminished expression of Bvg-repressed antigens and decreased transcription of Bvg-repressed genes. In contrast, mutation of risS had no effect on the expression of Bvg-regulated molecules. Mutation of risA also resulted in decreased bacterial invasion in a HeLa cell model. However, decreased invasion could not be attributed to the decreased expression of Bvg-repressed products, suggesting that mutation of risA may affect the expression of a variety of genes. Unlike the risAS operons in B. parapertussis and B. bronchiseptica, B. pertussis risS is a pseudogene that encodes a truncated RisS sensor. Deletion of the intact part of the B. pertussis risS gene does not affect the expression of risA-dependent, Bvg-repressed genes. These observations suggest that RisA activation occurs through cross-regulation by a heterologous system.
اللغةen
الناشرAmerican Society for Microbiology
الموضوعpertussis.
Bordetella pertussis.
Pertussis vaccine--Toxicity.
Bordetella pertussis--Immunology.
Bordetella pertussis--Pathogenicity.
العنوانBordetella pertussis risA, but not risS, is required for maximal expression of Bvg-repressed genes
النوعArticle
ESSN1098-5522
dc.accessType Open Access


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