> Thesis Defense Announcement
> To:  The George Mason University Community
> *Candidate: Sarah Hamer
> Program: Master of Science in Biology
> *
> *Date:   Wednesday April 25, 2012
> Time:   10:00 a.m.
> Place:  George Mason University, Prince William campus <http://www.gmu.edu/resources/visitors/findex.html>
> 	     Bull Run Hall, Room 247
> *Thesis Chair:  Dr. Serguei Popov
> Thesis Director: Dr. Myung-Chul Chung
> Title: "The S-nitrosylation of Peroxiredoxin 1 in Human Small Airway Epithelial Cells During Bacillus Anthracis Infection"
> A copy of the thesis is on reserve in the Johnson Center Library, 
> Fairfax campus.  The thesis will not be read at the meeting, but 
> should be read in advance. All members of the George Mason University 
> community are invited to attend.
> *Bacillus anthracis, a Gram-positive soil organism, is the causative 
> agent of anthrax.  Although the key virulence factor of anthrax is 
> mediated by toxins (i.e. lethal toxin and edema toxin), it has proven 
> that the bacterial nitric oxide synthase (bNOS) of B. anthracis, also, 
> plays a role in pathogenesis.  Since B. anthracis infection produced 
> bona fide nitric oxide that is responsible for protein modification by 
> S-nitrosylation,  I hypothesized that bNOS-induced nitric oxide 
> contributes to regulation of host cell function through protein 
> chemical modification.  The nitrosproteomic analysis using the 
> biotin-switch assay demonstrated that during B. anthracis infection, 
> peroxiredoxin 1 (Prx1) was predominantly S-nitrosylated; there was a 
> decrease in its peroxidase activity and an increase in its chaperone 
> activity, which both affect cell viability.  Treatment with a nitric 
> oxide donor in a high hydrogen peroxide environment decreased cell 
> viability; while during B. anthracis there was an increase in cell 
> viability, presumably due to increase of chaperone activity of Prx1.  
> These results suggest that during B. anthracis infection, 
> bacteria-derived nitric oxide plays a role in oxidative or nitrosative 
> stress-induced epithelial responses to the pathogen in the lung.
> //
> ###**