Linking dynamic signaling events within the same cell

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• John Albeck (University of California, Davis)
• Tuesday 05 April 2016, 14:00-14:45
• Seminar Room 1, Newton Institute.

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SDBW03 - Advances in numerical and analytic approaches for the study of non-spatial stochastic dynamical systems in molecular biology

In intracellular signaling pathways, biochemical activation events are transmitted from one node within the signaling network to another.  Recent work examining the information capacity of signaling pathways has concluded that most signaling pathways have limited abilities to resolve different strengths of inputs.  However, these studies are based on data in which only a single signal is measured in each cell, in response to a given cell, with the limitation that transmission of a signal from one signaling node to another cannot be directly observed.  Other published data suggest that single cells may have a much higher capacity to transmit quantitative information, which is obscured by population heterogeneity.  To better understand the properties of information transmission through biochemical cascades in individual cells, we have developed a panel of live-cell reporters to monitor multiple signaling events in the cell proliferation and growth network (CPGN).  These reporters include activity biosensors for the kinases ERK , Akt, mTOR, and AMPK , and CRISPR -based reporters for ERK target gene expression.  Experimental analysis with these tools reveals the temporal and quantitative linkage properties between nodes of the CPGN .  I will discuss two studies currently underway in our lab.  The first examines the how the CPGN manages the interplay between ATP -producing and ATP -consuming processes during cell proliferation; we find that loss of Akt signaling results in unstable levels of ATP and NADH in proliferating cells.  The second project focuses on how variations in amplitude and duration of ERK activity control the expression of the target gene Fra-1, which is involved in metastasis; here, we show that cancer therapeutics directed at inhibiting this pathway create strikingly different kinetics of ERK activity at the single-cell level, with distinct effects on Fra-1 expression.

This talk is part of the Isaac Newton Institute Seminar Series series.

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