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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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Siu Ng (Michael) from Dr. Hammer's lab will be presenting next week:
Title: Identifying the Regulation and Role of Vibrio cholerae Type VI Secretion System in Environmental Settings
Abstract: The Type VI secretion system (T6SS) is commonly used by Gram-negative bacteria to deliver toxic effectors into neighboring cells by direct contact. This competition mechanism has been shown to be important in inter-bacterial and host-microbe interactions. Vibrio cholerae is a waterborne pathogen resides in aquatic environments and the human gut. In response to environmental signals, including quorum sensing molecules and chitin, the QstR regulator activates the T6SS in clinical isolates like C6706. The TfoY regulator is required for T6SS activity in a human isolate V52. We sequenced dozens of V. cholerae environmental strains, and deletion of qstR and tfoY from many of the strains, including 3223-74, did not reduce T6SS killing efficiency in standard lab condition. We developed the first T6SS GFP transcriptional fusion to monitor T6 expressions in C67 or 3223-74 strains. To determine if 3223-74 T6SS is constitutive, the T6SS GFP reporters were introduced into E. coli, the results showed the reporters were not expressed, indicating both C67 and 3223-74 T6 promoters were inactive in E. coli, and thus, not constitutive. In addition, we also replaced C6706 T6 promoter on the genome with 3223-74 promoter (C6706swap). In C6706swap, T6SS was repressed when qstR was constitutive (qstR*) but de-repressed in the absence of qstR, and this is the opposite in the parental C6706. We hypothesize the change in T6SS expression is due to a QstR activating T6 repressor in C6706 that works on 3223-74 T6 promoter, but the repressor has a mutation and thus, defective in 3223-74. To understand how the 3223-74 T6SS is repressed in C6706, we are following two approaches: 1) 3223-74 transposon mutants is being screened to identify mutants in candidate activator that do not express a T6-GFP fusion and cannot kill target cells. 2) similar to 1), qstR* C6706swap transposon mutants is being screened to identify mutants in candidate repressor. 3) Alternatively, we use Aeromonas that constitutively expresses GFP as a target to determine if killing is restored due to the loss of T6 repressor.
