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Dr. Carlos Blondel
Department of Microbiology and Immunobiology, Harvard Medical School Division of Infectious Diseases Brigham and Women’s Hospital, Moston MA

Anfitrión: Dr. Francisco Chávez

The advent of CRISPR/Cas-based technology for disrupting protein coding genes is revolutionizing our capacity to comprehensively interrogate gene function in higher eukaryotes and it corresponds to an invaluable new approach to the study of host-pathogen interactions through functional genomics. Type III secretion systems (T3SSs) mediate injection of bacterial effector proteins into host cells and underlie the virulence of many Gram-negative pathogens. Decades of study have illuminated the bacterial factors required for T3SS function, but the host processes required for T3SS function remain largely undefined. I coupled CRISPR/Cas9 genome editing technology with the potent cytotoxicity of Vibrio parahaemolyticus’ two T3SSs (T3SS1 and T3SS2) to identify disruptions in the human genome that confer resistance to T3SS-dependent cytotoxicity. Surprisingly, absence of distinct host factors protected intestinal epithelial cells from the different T3SSs of this enteric pathogen. Genetic ablation of cell surface sulfation altered the kinetics of T3SS1-mediated cytotoxicity, while ablation of cell surface fucosylation abolished T3SS2-dependent killing. These observations illustrate the utility of genome-wide CRISPR/Cas9 screens for discovery of host processes underlying complex host-pathogen interactions.

Miércoles 23 de marzo de 2016, a las 12:00 horas.
Auditorio Prof. Hermann Niemeyer F., Edificio Biología Milenio.