University of California, Irvine (Irvine, CA)
Center for Infectious Diseases and Vaccinology
Biodesign Institute at Arizona State University (Tempe, AZ)
One possible persistence mechanism we are currently studying are toxin-antitoxin (TA) modules in the etiologic agent of tuberculosis. We have recently characterized a TA module belonging to the Rel TA module family: RelBE, RelFG, and RelJK. We have shown in Mycobacterium smegmatis that when the toxin is over-expressed, growth is inhibited. However this phenotype can be reversed when the cognate anti-toxin is also expressed, thus sufficiently neutralizing the growth inhibitory effects of the toxin.
2007 Teaching assistant in bacterial genetics laboratory course in SoLS.
2003-2004 Promotions photographer for Big City Radio/The Edge 103.9fm

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