Research Lecture at Nobel Forum
Date: 13 October, kl. 16.30
Speaker: Michael J. Berridge, The Babraham Institute, University of Cambridge, Cambridge, UK
Title: “Inositol trisphosphate, calcium and Vitamin D signalling in health and disease”
Many cellular functions are regulated by calcium (Ca2+) signals that are generated by different signalling pathways. One of these is the inositol trisphosphate/calcium (InsP3/Ca2+) signalling pathway that operates through either primary or modulatory mechanisms. In its primary role, it generates the Ca2+ that acts directly to control many cellular processes. Its modulatory role occurs in excitable cells where it modulates the primary Ca2+ signal generated by the entry of Ca2+ through voltage-operated channels. In carrying out this modulatory role, the InsP3/Ca2+ signalling pathway induces subtle changes in the generation and function of the voltage-dependent primary Ca2+ signal. Changes in the nature of both the primary and modulatory roles of InsP3/Ca2+ signalling are a contributory factor responsible for the onset of many human pathologies such as Alzheimer’s disease and heart disease. Many of these diseases can be prevented by Vitamin D that acts to maintain Ca2+ homeostasis.
The Nobel Prize in Physiology or Medicine will be announced Monday October 3 at 11.30 at earliest, Nobel Forum, Nobels väg 1, 171 77 Stockholm.
Registration and press id is required to attend the Press Conference.
When the Secretary General begins his announcement at the Press Conference, the following information material will become available at www.nobelprizemedicine.org and at www.nobelprize.org:
- Open webcast from the Press Conference
• Press releases in English and Swedish
• Scientific background in English
• Illustrations, web links and further reading
At the venue several experts will be available for interviews in Swedish or English (5-10 minutes), please indicate in the registration.
Research Lecture at Nobel Forum
15 September, kl. 16.30
Bonnie L. Bassler
Professor in Molecular Biology
Department of Molecular Biology, Princeton University New Jersey, USA
Title: “Quorum Sensing and its Control”
Bacteria communicate with one another via the production and detection of secreted signal molecules called autoinducers. This cell-to-cell communication process, called “Quorum Sensing”, allows bacteria to synchronize behavior on a population-wide scale. Behaviors controlled by quorum sensing are usually ones that are unproductive when undertaken by an individual bacterium acting alone but become effective when undertaken in unison by the group. For example, quorum sensing controls virulence factor production, biofilm formation, and the excretion of public goods such as enzymes that solubilize solid food sources making them accessible for consumption. We developed small molecule quorum-sensing agonists and antagonists to discover the principles underlying the exquisite selectivity quorum-sensing receptors have for their cognate ligands. Our results suggest mechanisms bacteria use in the wild to ensure the proper ligand has interacted with its partner receptor prior to eliciting signal transduction. We suggest that, in their native environments, bacteria encounter mixtures of autoinducers produced by other species occupying the same niche. Precise autoinducer discrimination enables a particular species of bacteria to respond exclusively to its own signal even in the face of fierce competition. This ability prevents the leakage of benefits of quorum-sensing-controlled public goods to non-kin. Beyond learning about fundamental principles underlying quorum sensing, another use for our synthetic molecules is to control quorum sensing on demand. Indeed, our most potent quorum sensing antagonist protects animals from quorum-sensing-mediated killing by pathogenic bacteria and prevents biofilm formation in model microfluidics chambers that mimic medical devices. These results validate the notion that targeting quorum sensing has potential for antimicrobial drug development.