Lecture Archive

/Lecture Archive

Nobel Laureate Revisiting Lecture – Jack Szostak

Nobel Laureate Revisiting Lecture

Jack Szostak, Nobel Laureate in Physiology or Medicine 2009
Wednesday, April 15th at 16.30

Title: “The Origins of Cellular Life”
Primitive cells consisting of a self-replicating nucleic acid genome encapsulated within a self-replicating membrane would have depended upon a rich, complex and variable environment to drive their reproduction. I will describe simple and robust pathways for the coupled growth and division of primitive cell membranes composed of fatty acids and related single-chain amphiphiles. I will also discuss recent progress towards the efficient and accurate chemical replication of RNA, including possible roles for short peptides. Chemical template-copying generally proceeds best at low temperatures, but strand separation requires transient exposure to high temperatures, which would also facilitate the entry of nutrients into primitive cells. Taken together, these chemical and physical considerations favor an origin of life scenario involving ponds or lakes in a geothermally active environment.

Venue: Wallenbergsalen, Nobel Forum,
Karolinska Institutet, Nobels väg 1
Host: Professor Rune Toftgård Rune.Toftgard@ki.se
Contact: Ann-Mari Dumanski, Nobel Office, Nobel Forum
08-524 878 00, Ann-Mari.Dumanski@nobel.se

Karolinska Research Lectures – Michael Lynch

Karolinska Research Lectures at NOBEL FORUM
April 16, 16.30

Michael Lynch
Department of Biology, Indiana University, Bloomington, USA

Title: Mutation, Drift, and the origin or subcellular features

Although natural selection may be the most powerful force in the biological world, it is not all powerful. As a consequence, many aspects of evolution of the molecular level can only be explained by the inability of natural selection to operate. This general principle explains a lot about the evolution of genome architecture, and also appears to extend to multiple higher-level features of cells, as most clearly demonstrated with observations on replication fidelity.
Understanding the mechanisms of evolution and the degree to which phylogenetic generalities exist requires information on the rate at which mutations arise and their effects at the molecular and phenotypic levels. Although procuring such data has been technically challenging, high-throughput genomic sequencing is rapidly expanding our knowledge in this area. Most notably, information on spontaneous mutations, now available in a wide variety of organisms, implies an inverse scaling of the mutation rate (per nucleotide site) with the effective population size of a lineage. The argument will be made that this pattern naturally arises as natural selection pushes the mutation rate down to a lower limit set by the power of random genetic drift rather than by intrinsic molecular limitations on repair mechanisms or by selection for an optimum mutation rate.

This drift-barrier hypothesis has general implications for all aspects of evolution, including the performance of enzymes, the stability of proteins, and the refinement of transcription-factor binding sites. The fundamental idea here is that as molecular adaptations become more and more refined, the room for subsequent improvement becomes diminishingly small. If this hypothesis is correct, the population-genetic environment imposes a fundamental constraint on the level of perfection that can be achieved by any molecular adaptation, and indeed all adaptations. Additional examples consistent with this hypothesis will be drawn from recent observations on the transcription-error rate and on the evolution of the oligomeric states of proteins.

Host: Jussi Taipale, Karolinska Institutet, email: jussi.taipale@ki.se

Contact: Tatiana Goriatcheva, Nobel Office, Nobel Forum,
tel. 524 87805, tatiana.goriatcheva@nobel.se

Karolinska research lecture – Junying Yuan

Karolinska Research Lectures at NOBEL FORUM

March 19, 16.30

Junying Yuan
Department of Cell Biology, Harvard Medical School, Boston, USA


Title: “Regulation of necroptosis and inflammation by RIPK1”

Necrosis is a common pathological feature in a multitude of human diseases ranging from cancers to neurodegeneration. However, the traditional belief that necrosis was a passive form of cell death caused by overwhelming stress has stymied research in this area as well as impeded the development of therapeutic methods targeting necrosis. We demonstrated that TNFa, an important proinflammatory cytokine, could activate a regulated necrotic cell death mechanism – termed necroptosis – and developed specific small molecule inhibitors of necroptosis, the necrostatins. A chemically improved Necrostatin-1 (Nec-1) analog, R-7-Cl-O-Nec-1, turned out to be a highly specific inhibitor of the kinase activity of RIPK1. The ability of Nec-1 and its analogues to inhibit necrosis in many cultured models as well as animal models of human diseases overturned the traditional dogma of necrosis as passive cell death and led to the rapid acceptance and explosion of research on necroptosis. RIPK1 has emerged as a key upstream regulator that controls necroptosis, inflammatory signaling as well as certain specific forms of apoptosis. The ability of RIPK1 to modulate these key cellular events is tightly controlled by phosphorylation and the interaction with its downstream mediators. Targeting RIPK1 might provide an exciting novel therapeutic strategy for the treatment of both acute and chronic human diseases.

Host:Boris Zhivotovsky & Helin Norberg, Karolinska Institutet

Contact:Tatiana Goriatcheva, Nobel Office, Nobel Forum,
tel. 524 87805, tatiana.goriatcheva@nobel.se


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