Tuberculosis infects roughly one third of the world population and is a global health concern. The ability of pathogenic mycobacteria to arrest phagosome maturation and establish an intracellular niche within the host macrophage is a hallmark of the infection. The mechanism by which this occurs is not well understood. It is hypothesized that M. tuberculosis actively secretes effectors involved in the arrest of phagosome maturation. Such factors could be protein or lipid kinases that would be delivered to the phagosome lumen where they could target and modulate normal host signaling and intracellular trafficking. The goal of this project is to identify M. tuberculosis effector kinases.
The specific aims of this proposal are: 1. The identification of ATP-hydrolyzing enzymes secreted by M. tuberculosis and associated with the M. tuberculosis vacuole. 2. Assessing the activity of recombinant effector proteins on the host cell. ? ? ?

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32AI066537-02
Application #
7274208
Study Section
Special Emphasis Panel (ZRG1-F13-P (20))
Program Officer
Jacobs, Gail G
Project Start
2006-08-01
Project End
2008-07-31
Budget Start
2007-08-01
Budget End
2008-07-31
Support Year
2
Fiscal Year
2007
Total Cost
$52,048
Indirect Cost
Name
Cornell University
Department
Microbiology/Immun/Virology
Type
Schools of Veterinary Medicine
DUNS #
872612445
City
Ithaca
State
NY
Country
United States
Zip Code
14850
Purdy, Georgiana E; Russell, David G (2007) Lysosomal ubiquitin and the demise of Mycobacterium tuberculosis. Cell Microbiol 9:2768-74