Events - Weekly
|Sunday, April 28|
|Monday, April 29|
David Rand, Warwick U, Design principles and dynamics in clocks, cell cycles and signals
I will review three recent pieces of work that bring out different aspects of System Biology research that I am involved in e.g. modelling, tools/algorithms for analysis of imaging, transcriptomics and other data, analytical tools & techniques for understanding design principles. I will discuss three topics. Firstly, coupling of the circadian clock and cell cycle in mammalian cells. Secondly, a radical revision of the Nrf2 signalling system. Stress responsive signalling coordinated by Nrf2 provides an adaptive response for protection against toxic insults, oxidative stress and metabolic dysfunction. Thirdly, the question of what lies behind temperature compensation of circadian clocks. Temperature compensation, one of the key themes of circadian biology, is about the constancy or near-constancy of the free-running period under changing temperature but it is not clear how evolution acts on the free-running period since in physiological conditions the clock is entrained to the day–night cycle and therefore has a constant period of 24 h. It therefore seems reasonable to hypothesise that temperature compensation for the free-running clock is a consequence of the selective pressure on some other aspect of the entrained circadian clock. I will use new experimental data and mathematical results to suggest a resolution this question.
Joseph Henry Room, Jadwin Hall · 12:00 p.m.– 1:00 p.m.
Joseph Nadeau, Pacific Northwest Diabetes Institute, Here be dragons: heritable epigenetic origins of phenotypic variation and disease risk
Both humans and animal models provide many examples of highly heritable traits where the disease-causing genetic variants elude discovery. In these cases, heritability is often high but the explained genetic variance is low. The usual explanation involves undetected genetic variants with weak and heterogeneous actions in affected individuals. This explanation is reasonable given the limited statistical power in most genetic studies. However, we recently found several examples of heritable epigenetic changes, through the germline, suggesting that modes of inheritance other than DNA can also be transmitted across generations to affect phenotypic variation and disease risk. In each case, genetic variants in ancestral generations lead to phenotypic variation in subsequent generations. These effects can be as common and strong as those resulting from conventional inheritance, and they can persist for multiple generations. Transgenerational inheritance affects cancer, metabolic diseases, behaviors and many other traits. The effects are usually specific to one germ-lineage, with examples of transmission through the female germ-lineage and others through the paternal germ-lineage. The identity of the genes that mediate these effects implicate aspects of RNA biology including RNA editing, demethylation, translation control, and regulation of miRNA biology. These transgenerational effects challenge our understanding of inheritance and the origins of phenotypic variation and disease risk.
Carl Icahn Lab 101 · 4:15 p.m.– 5:15 p.m.
|Tuesday, April 30|
Erel Levine, Harvard Dept. of Physics, Many are called but few are chosen: the targets of small RNAs
Department of Physics and FAS Center for Systems Biology Harvard University
Small regulatory RNAs play major roles in regulating cellular and organismic functions under normal conditions as well as in stress and disease. Target specificity is achieved via base-pairing of very short sequences, allowing hundreds of potential targets per small RNA. At the same time, molecular and cellular properties of a target have strong effect on the regulation efficacy in vivo. In this talk I'll describe some of these effects, and address the question how the regulation of many targets is coordinated in the cell.
Carl Icahn Lab 101 · 4:30 p.m.– 5:30 p.m.
|Wednesday, May 1|
|Thursday, May 2|
|Friday, May 3|
|Saturday, May 4|