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dc.creatorSchmidt, Sarah Louise
dc.date.accessioned2017-10-10T20:19:13Z
dc.date.available2017-10-10T20:19:13Z
dc.date.created2013-05
dc.date.issued2013-02-04
dc.date.submittedMay 2013
dc.identifier.urihttps://hdl.handle.net/1969.1/164412
dc.description.abstractClostridium difficile is a Gram-positive, anaerobic, spore-forming bacteria that is the leading cause of antibiotic-associated diarrhea. C. difficile infections (CDI) are thought to be caused by ingestion of spores by a host with an altered intestinal flora, often caused by antibiotic treatments for unrelated conditions. C. difficile spores germinate in vivo when exposed to bile acids, which are commonly toxic to bacterial pathogens, and glycine. The proliferation of the resulting vegetative cells suggests the presence of mechanism(s) to resist bile acid-mediated toxicity. Previous studies identified genes with altered mRNA abundance following bile acid exposure. The expression of C. difficile CD2118 increased 20-fold upon exposure to cholic acid or deoxycholic acid. C. difficile CD2118 encodes a putative ABC (ATP-binding cassette) transporter, a class of transporters known to participate in bile acid resistance mechanisms of other Gram-positive bacteria. Herein, we characterize the role of CD2118 in protecting C. difficile against bile acid-mediated toxicity by constructing a site-directed mutation in the coding region of C. difficile CD2118 using the TargeTron system.en
dc.format.mimetypeapplication/pdf
dc.subjectClostridium difficileen
dc.subjectbile aciden
dc.subjectresistance mechanismsen
dc.titleThe effect of CD2118 on Clostridium difficile bile acid resistanceen
dc.typeThesisen
thesis.degree.departmentBiologyen
thesis.degree.disciplineBiologyen
thesis.degree.grantorUndergraduate Research Scholars Programen
dc.contributor.committeeMemberSorg, Joseph A
dc.type.materialtexten
dc.date.updated2017-10-10T20:19:13Z


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