Free Technical Lecture: Bacterial Quorum Sensing and Virulence in Vibrio cholerae
Apr 10
(10 a.m. - 12 p.m.)
(10 a.m. - 12 p.m.)
Location:
TI Auditorium
TI Auditorium
Free Technical Lecture, Open to the Public (please park in Lot J, see: http://www.utdallas.edu/maps/)
Princeton Geneticist Dr. Bonnie Bassler uncovered a landmark discovery in the field of biology--bacteria actually communicate with each other. Called quorum sensing, this cell-to-cell communication plays a key role in diseases affecting plants, animals and humans. Dr. Bassler's research sparked new research into disease prevention and treatment.
Dr. Bassler was recognized as a MacArthur Foundation Fellow in 2002 and is the distinguished Anson L. Clark Memorial Lecturer for 2009.
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.
See website for more information
Please Note: The UT Dallas campus is undergoing a significant amount of construction. Guests are advised to visit our campus map for updated route, construction, and parking information.
Tagged as Lectures/Seminars
Princeton Geneticist Dr. Bonnie Bassler uncovered a landmark discovery in the field of biology--bacteria actually communicate with each other. Called quorum sensing, this cell-to-cell communication plays a key role in diseases affecting plants, animals and humans. Dr. Bassler's research sparked new research into disease prevention and treatment.
Dr. Bassler was recognized as a MacArthur Foundation Fellow in 2002 and is the distinguished Anson L. Clark Memorial Lecturer for 2009.
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.
See website for more information
Please Note: The UT Dallas campus is undergoing a significant amount of construction. Guests are advised to visit our campus map for updated route, construction, and parking information.
Tagged as Lectures/Seminars
