The CDF-type metal efflux protein EmfA is essential for Brucella abortus 2308 resistance to manganese toxicity and is a critical virulence determinant in experimentally-infected mice / by Matthew J. Johnsrude.

Author/creator Johnsrude, Matthew J. author.
Other author Roop, R. Martin, II, degree supervisor.
Other author East Carolina University. Department of Biology.
Format Theses and dissertations
Publication[Greenville, N.C.] : [East Carolina University], 2019.
Description99 pages : illustrations (chiefly color)
Supplemental ContentAccess via ScholarShip
Subjects

Summary Divalent cationic metals are important trace nutrients for all bacteria because metals serve as cofactors for proteins involved in numerous cellular functions. Despite the fact that metals play an essential role in bacterial physiology, metals become harmful to bacteria if accumulated in excess. To prevent metal-induced toxicity, bacteria employ a variety of factors, such as metal-responsive transcriptional regulators and metal efflux proteins, that function to maintain proper intracellular metal homeostasis. The Brucella strains are Gram-negative, pathogenic bacteria that cause the severe febrile zoonotic disease, brucellosis, and these bacteria require the metal manganese for growth and during host infection. While the manganese acquisition protein, MntH, is essential for the capacity of Brucella spp. to maintain sufficient manganese nutrition, the mechanisms by which these bacteria prevent manganese toxicity have not been determined. The studies of this thesis were performed to identify how Brucella spp. cope with manganese toxicity and whether these factors are essential for Brucella virulence.
General notePresented to the faculty of the Department of Biology
General noteAdvisor: R. Martin Roop II
General noteTitle from PDF t.p. (viewed October 15, 2019).
Dissertation noteM.S. East Carolina University 2019.
Bibliography noteIncludes bibliographical references.
Technical detailsSystem requirements: Adobe Reader.
Technical detailsMode of access: World Wide Web.

Availability

Library Location Call Number Status Item Actions
Electronic Resources Access Content Online ✔ Available