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035 a| (Sirsi) o869897685;

035 a| (OCoLC)869897685;

049 a| EREE;

100 1 a| Yerke, Aaron,e| author.?| UNAUTHORIZED;

245 14 a| The contribution of motility and chemotaxis in the Borrelia burgdorferi infectious life cycle /c| by Aaron Yerke.;

264 1 a| [Greenville, N.C.] :b| [East Carolina University],c| 2013.;

300 a| 87 pages :b| illustrations (some color);

336 a| textb| txt2| rdacontent;

337 a| computerb| c2| rdamedia;

338 a| online resourceb| cr2| rdacarrier;

347 a| text fileb| PDFc| 2.41Mb2| rda;

490 1 a| ECU Brody School of Medicine thesis;

500 a| Presented to the faculty of the Biomedical Sciences Program.;

538 a| System requirements: Adobe Reader.;

538 a| Mode of access: World Wide Web.;

502 b| M.S.c| East Carolina Universityd| 2013.;

500 a| Advisor: M.D. Motaleb.;

500 a| Title from PDF t.p. (viewed February 05, 2014).;

520 3 a| Lyme disease has emerged as an increasing problem for people in the east and northeastern part of the United States. It can cause a chronic debilitating infection if left untreated and is difficult to diagnose. The illness is caused by an infection with the spirochete known as Borrelia burgdorferi. B. burgdorferi is a Gram-negative bacterium that is transmitted by ticks of the Ixodes genus. The primary carriers in regions of high Lyme disease incidence are Ixodes scapularis vector and white-footed Mus musculus rodents. B. burgdorferi is not known to produce common virulence factors such as toxins or capsules. Chemotaxis and motility are important for B. burgdorferi to cause infection and are considered as invasive attributes of this organism. Only a handful of studies have reported that non-chemotactic and non-motile B. burgdorferi mutants are unable to disseminate in hosts, and are, therefore, non-infectious in mice. Although motility and chemotaxis has been shown to be crucial for the infectious life cycle of B. burgdorferi, little is known about the mechanism of motility or assembly of periplasmic flagella. It is not known how incremental reductions of motility affect B. burgdorferi's virulence. Recent cryo-electron microscopy tomography revealed that spirochetes possess a unique flagellar structure called the collar. However, the gene or genes that encode for the B. burgdorferi collar proteins are unknown. Because of its location in the periplasmic flagellar motor, we hypothesize that this organelle is important for flagellar assembly as well as motility. We also hypothesize that less motile or less chemotactic mutants will exhibit a reduced invasive phenotype in vivo. Using Bioinformatics techniques, two potential candidate genes were identified (bb0526 and bb0773) that may encode the collar. These two genes are annotated as putative genes in the B. burgdorferi genome with no significant similarity to other bacterial species outside of spirochetes. A BLAST search indicated that bb0526 has homology to an unconfirmed motility gene in Treponema pallidum, another spirochete. A third gene, fliZ, putatively encodes a regulator of the flagella assembly complex. In other bacteria, inactivation of fliZ creates a reduced motile phenotype. Two genes that are hypothesized to have chemotactic function are cheY1 and cheY2. Inactivation of these genes creates mutants with a phenotype indistinguishable from wild type in vitro. However, they may exhibit a different phenotype in vivo. In order to test our hypotheses, mutants for cheY1, cheY2, bb0526, bb0773, and fliZ were created. Our results show that the [delta]bb0773 mutant exhibits no discernible defects with respect to motility or morphology; the [delta]bb0526 mutant is associated with the collar structure and has a decreased motility defect. Inactivation of fliZ creates a mutant with a reduced number of periplasmic flagella and the wild type phenotype is restored upon complementation in trans. To demonstrate if reduced motility or chemotaxis is important for survivability or transmission between hosts, we plan to assay these mutants in mouse-tick-mouse infection cycle experiments.;

504 a| Includes bibliographical references.;

650 2 a| Lyme Disease.=| ^A925335;

650 2 a| Ticks.=| ^A922347;

650 2 a| Ixodes.=| ^A1065947;

650 2 a| Tick-Borne Diseases.=| ^A943323;

650 2 a| Erythema Chronicum Migrans.=| ^A964420;

650 2 a| Borrelia burgdorferix| pathogenicity.=| ^A1195262;

650 2 a| Chemotaxis.=| ^A1195179;

650 2 a| Mice.=| ^A921375;

650 2 a| Treponema pallidum.=| ^A1195239;

650 2 a| Gram-Negative Anaerobic Bacteria.=| ^A1195193;

650 2 a| Gram-Negative Bacterial Infections.=| ^A931426;

650 2 a| Borrelia Infections.=| ^A964305;

653 a| Molecular biology;

700 1 a| Motaleb, M.D.,e| degree supervisor.?| UNAUTHORIZED;

710 2 a| Brody School of Medicine.b| Office of Research and Graduate Studies.b| Biomedical Sciences. ?| UNAUTHORIZED;

830 0 a| ECU Brody School of Medicine thesis.=| ^A964744;

856 40 z| Access via ScholarShipu| http://hdl.handle.net/10342/4328;

949 a| Click on web addressw| ASISh| JOYNER101;

949 a| Click on web addressw| ASISh| HSL111;

994 a| C0b| ERE;

096 a| WC 406;

596 a| 1 4;

998 a| 3422710;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 3422710-1001l| JNETm| JOYNERr| Ys| Yt| JNE3ETDu| 2/5/2014x| ETDz| JERESOURCE;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 3422710-2001l| HSLELECm| HSLr| Ys| Yt| HEETDu| 2/5/2014x| ETDz| HERESOURCE;

The contribution of motility and chemotaxis in the Borrelia burgdorferi infectious life cycle / by Aaron Yerke.

Author/creator	Yerke, Aaron author.
Other author	Motaleb, M.D., degree supervisor.
Other author	Brody School of Medicine. Office of Research and Graduate Studies. Biomedical Sciences.
Format	Theses and dissertations
Publication	[Greenville, N.C.] : [East Carolina University], 2013.
Description	87 pages : illustrations (some color)
Supplemental Content	Access via ScholarShip
Subjects	Lyme Disease. Ticks. Ixodes. Tick-Borne Diseases. Erythema Chronicum Migrans. Borrelia burgdorferi--pathogenicity. Chemotaxis. Mice. Treponema pallidum. Gram-Negative Anaerobic Bacteria. Gram-Negative Bacterial Infections. Borrelia Infections.

Series	ECU Brody School of Medicine thesis ECU Brody School of Medicine thesis. ^A964744
Summary	Lyme disease has emerged as an increasing problem for people in the east and northeastern part of the United States. It can cause a chronic debilitating infection if left untreated and is difficult to diagnose. The illness is caused by an infection with the spirochete known as Borrelia burgdorferi. B. burgdorferi is a Gram-negative bacterium that is transmitted by ticks of the Ixodes genus. The primary carriers in regions of high Lyme disease incidence are Ixodes scapularis vector and white-footed Mus musculus rodents. B. burgdorferi is not known to produce common virulence factors such as toxins or capsules. Chemotaxis and motility are important for B. burgdorferi to cause infection and are considered as invasive attributes of this organism. Only a handful of studies have reported that non-chemotactic and non-motile B. burgdorferi mutants are unable to disseminate in hosts, and are, therefore, non-infectious in mice. Although motility and chemotaxis has been shown to be crucial for the infectious life cycle of B. burgdorferi, little is known about the mechanism of motility or assembly of periplasmic flagella. It is not known how incremental reductions of motility affect B. burgdorferi's virulence. Recent cryo-electron microscopy tomography revealed that spirochetes possess a unique flagellar structure called the collar. However, the gene or genes that encode for the B. burgdorferi collar proteins are unknown. Because of its location in the periplasmic flagellar motor, we hypothesize that this organelle is important for flagellar assembly as well as motility. We also hypothesize that less motile or less chemotactic mutants will exhibit a reduced invasive phenotype in vivo. Using Bioinformatics techniques, two potential candidate genes were identified (bb0526 and bb0773) that may encode the collar. These two genes are annotated as putative genes in the B. burgdorferi genome with no significant similarity to other bacterial species outside of spirochetes. A BLAST search indicated that bb0526 has homology to an unconfirmed motility gene in Treponema pallidum, another spirochete. A third gene, fliZ, putatively encodes a regulator of the flagella assembly complex. In other bacteria, inactivation of fliZ creates a reduced motile phenotype. Two genes that are hypothesized to have chemotactic function are cheY1 and cheY2. Inactivation of these genes creates mutants with a phenotype indistinguishable from wild type in vitro. However, they may exhibit a different phenotype in vivo. In order to test our hypotheses, mutants for cheY1, cheY2, bb0526, bb0773, and fliZ were created. Our results show that the [delta]bb0773 mutant exhibits no discernible defects with respect to motility or morphology; the [delta]bb0526 mutant is associated with the collar structure and has a decreased motility defect. Inactivation of fliZ creates a mutant with a reduced number of periplasmic flagella and the wild type phenotype is restored upon complementation in trans. To demonstrate if reduced motility or chemotaxis is important for survivability or transmission between hosts, we plan to assay these mutants in mouse-tick-mouse infection cycle experiments.
General note	Presented to the faculty of the Biomedical Sciences Program.
General note	Advisor: M.D. Motaleb.
General note	Title from PDF t.p. (viewed February 05, 2014).
Dissertation note	M.S. East Carolina University 2013.
Bibliography note	Includes bibliographical references.
Technical details	System requirements: Adobe Reader.
Technical details	Mode of access: World Wide Web.

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The contribution of motility and chemotaxis in the Borrelia burgdorferi infectious life cycle / by Aaron Yerke.

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