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There is now a CONTENT FREEZE for Mercury while we switch to a new platform. It began on Friday, March 10 at 6pm and will end on Wednesday, March 15 at noon. No new content can be created during this time, but all material in the system as of the beginning of the freeze will be migrated to the new platform, including users and groups. Functionally the new site is identical to the old one. webteam@gatech.edu
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Abstract: Vibrio cholerae, the causative agent of the intestinal disease cholera, interacts with other bacteria in multi-species communities in host and environmental settings. Using the harpoon-like type VI secretion system (T6SS), V. cholerae delivers toxic proteins into neighboring cells, causing lysis. A V. cholerae strain that constitutively expresses T6SS genes can effectively kill target species Escherichia coli, Aeromonas, and T6SS-sensistive V. cholerae cells. I found that addition of glucose to a standardized killing assay against V. choleraerestores E. coli survival but does not restore Aeromonas or T6SS-sensitive V. cholerae survival. A growth assay revealed that E. colidoubling time does not affect killing by V. cholerae. Additional evidence suggests E. coli does not produce a diffusible molecule that represses the T6SS of V. cholerae. Investigation by fluorescence microscopy revealed that E. coli cells survive in glucose even when entirely surrounded by V. cholerae cells, which implies that glucose causes a relevant physiological change in individual E. coli cells. We propose that further studies should focus on the E. coli capsule as a potential mechanism for surviving T6SS attacks. This study makes an unprecedented case that the outcome of microbial warfare via the T6SS can be dependent on nutrient availability.
