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The Anson L. Clark Memorial Lecture

began in 1970 and has drawn distinguished speakers to the UT Dallas campus every year since. The lecture honors the memory of a remarkable individual who amassed a sizeable fortune throughout a highly unusual and successful career – first, as an engineer, then as a physician at the Mayo Clinic and finally as a businessman in the oil and banking industries.

Clark’s philanthropic activities have for many decades supported scholarly endeavors at a number of Texas colleges and universities, including the Clark Summer Research Program and the Clark Presidential Scholarship at UT Dallas.

Small Talk: Cell-to-Cell Communication in Bacteria
2009 Annual Anson L. Clark Memorial Lecture

Princeton Geneticist Dr. Bonnie Bassler discovered a secret about bacteria that the scientific world had missed--bacteria talk to each other!

This process, called quorum sensing, enables bacteria to successfully infect and cause disease in plants, animals, and humans. The discovery has lead to new research that may help create new ways to fight infection.

Dr. Bassler is a recipient of the MacArthur "genius" award and has been elected to the National Academy of Sciences.

Bacterial Quorum Sensing and Virulence in Vibrio Cholerae,
Technical Presentation (Free and Open to the Public)

Technical Abstract:

Vibrio cholerae El Tor, the etiological agent of the current cholera pandemic uses cell-to-cell communication to control pathogenicity and biofilm formation. This process, called quorum sensing, relies on the secretion and detection of signaling molecules called autoinducers. At low cell density, V. cholerae activates virulence factor expression and biofilm formation. At high cell density, the accumulation of two quorum-sensing autoinducers (CAI-1 and AI-2) represses these traits. Autoinducer information is transduced to multiple small regulatory RNAs (sRNAs) that lie at the heart of the V. cholerae El Tor quorum sensing cascade. The sRNAs base-pair with, and repress the translation of, the mRNA encoding the master transcriptional regulator, HapR. We have identified a new sRNA-dependent, HapR-independent quorum sensing pathway. Classical V. cholerae, which caused previous pandemics and is reportedly incapable of quorum sensing due to a nonfunctional HapR, exhibits quorum sensing-controlled gene expression through this new HapR-independent pathway. The two V. cholerae autoinducers, CAI-1 and AI-2, function synergistically to control gene regulation, although CAI-1 is the stronger of the two signals. We purified and identified CAI-1 as (S)-3-hydroxytridecan-4-one, a new type of bacterial autoinducer. Synthetic (S)-3-hydroxytridecan-4-one functions as well as natural CAI-1 in repressing production of the canonical virulence factor toxin co-regulated pilus (TCP). Our findings suggest that CAI-1 could be used as a therapy to prevent cholera infection and, furthermore, that strategies to manipulate bacterial quorum sensing hold promise in the clinical arena.

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  • Updated: April 8, 2009