Paula I. Watnick

Division of Infectious Diseases

Department of Pediatrics

Children's Hospital Boston
Enders Building, Room 760
300 Longwood Avenue
Boston, MA 02115
Tel: (617) 919-2918
Fax: (617) 730-0254
Email: paula.watnick@childrens.harvard.edu

5 postdoctoral fellows, 1 technician

Vibrio cholerae is a marine organism, a symbiont of arthropods, and a pathogen of humans that causes severe and pandemic diarrheal disease. V. cholerae survives in the aquatic environment through adhesion to the surfaces of particulates, plants, and insects. When ingested, V. cholerae passes through the human gastrointestinal tract to colonize the distal small intestine and colon. Cholera toxin, which is secreted into the intestinal lumen, is taken up by intestinal epithelial cells where it activates adenylate cyclase leading to opening of cAMP-responsive ion channels. Our laboratory investigates the strategies V. cholerae uses to colonize aquatic surfaces, the arthropod intestine, and the mammalian intestine.

1) Environmental signals that induce biofilm formation. Our laboratory has identified multiple environmental signals that activate Vibrio cholerae biofilm formation. We are currently dissecting the signal transduction cascades that sense these signals.

2) The host-pathogen interaction using a Drosophila model. Ingestion of pathogenic V. cholerae by Drosophila melanogaster induces an infection with many similarities to cholera. We use the powerful genetic tools available in the fly to identify components of the innate immune system that modulate susceptibility to disease.

3) Interaction of Vibrio cholerae with the commensal microbiota of the intestine. Colonization of the mammalian intestine is the first step in V. cholerae infection. We hypothesize that our commensal microbiota protects us against this infection. Our laboratory uses a germ-free mouse model to study the genetics of V. cholerae intestinal colonization in the presence and absence of commensal microbiota.

References:

Blow N, Watnick PI, Vibrio cholerae infection of Drosophila melanogaster mimics the human disease cholera, PLoS Pathogens, 2005; 1:92-98.
Berkey C, Blow N, Watnick PI, Genetic analysis of Drosophila melanogaster susceptibility to intestinal V. cholerae infection. Cell Microbiol. 2009; 11:461-474.
Karatan E, Watnick P, Signals, regulatory networks and materials that build and break bacterial biofilms, Microbiol Mol Biol Rev. 2009;73:310-347.
Houot L. Chang S. Absalon C, Watnick PI, Vibrio cholerae PTS control of carbohydrate transport, biofilm formation, and colonization of the germ-free mouse intestine, Infect Immun, 2010; 78:1482-94.
Houot L, Chang S., Pickering BS, Absalon C, Watnick, PI, The PTS regulates Vibrio cholerae biofilm formation through multiple independent pathways, J Bacteriol, 2010 192: in press.

BBS webpage updated 5/7/2010