Dr. Woodward performed his graduate studies in the Department of Chemistry at the University of California, Berkeley with Dr. Michael Marletta studying the biochemistry of nitric oxide synthase. As a postdoctoral fellow at University of California, Berkeley with Dr. Daniel Portnoy he studied host detection of Listeria moncytogenes.
Research in the Woodward laboratory is focused on elucidating the interactions of bacteria with their hosts that lead to the development of pathological states. We utilize the gram-positive intracellular bacterium Listeria monocytogenes as a genetically tractable model to define (i) the molecular features that allow access and adaptation of bacteria to the host intracellular niche and (ii) the host response to bacteria on the outcome of infection. To this end we have recently identified the novel bacterial nucleotide cyclic di-AMP as the molecule recognized by the infected host during L. monocytogenes entry into the host cell cytosol. C-di-AMP is a recently discovered bacterial signaling molecule that is highly conserved among many bacteria that interact with eukaryotic hosts, although its function in these microbes generally remains unknown. We utilize a diverse array of techniques including bacterial genetics, biochemistry, mass spectrometry, proteomics, cell culture and in vivo models of infection to further interrogate the mechanisms of cytosolic immuno-surveillance as well as the roles of c-di-AMP in bacterial physiology.
Woodward J.J., Iavarone A.T., Portnoy D.A. “c-di-AMP secreted by intracellular Listeria monocytogenes activates a host type I interferon response.” Science. (2010) 328, 1703-5.
Sauer J.D., Sotelo-Troha K., von Moltke J., Monroe K.M., Rae C.S., Brubaker S.W., Hyodo M., Hayakawa Y., Woodward J.J., Portnoy D.A., Vance R.E. “The ENU-induced Goldenticket (Gt) mouse mutant reveals an essential function of Sting (Tmem173, Mita, Mpys, Eris) in the in vivo interferon response to Listeria monocytogenes and cyclic-di-nucleotides.” Infection and Immunity. (2011) 79, 688-94.