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Frequency modulation of ERK activation dynamics rewires cell fate
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Journal Article
Frequency modulation of ERK activation dynamics rewires cell fate
2015
Overview
Transient versus sustained ERK MAP kinase (MAPK) activation dynamics induce proliferation versus differentiation in response to epidermal (EGF) or nerve (NGF) growth factors in PC‐12 cells. Duration of ERK activation has therefore been proposed to specify cell fate decisions. Using a biosensor to measure ERK activation dynamics in single living cells reveals that sustained EGF/NGF application leads to a heterogeneous mix of transient and sustained ERK activation dynamics in distinct cells of the population, different than the population average. EGF biases toward transient, while NGF biases toward sustained ERK activation responses. In contrast, pulsed growth factor application can repeatedly and homogeneously trigger ERK activity transients across the cell population. These datasets enable mathematical modeling to reveal salient features inherent to the MAPK network. Ultimately, this predicts pulsed growth factor stimulation regimes that can bypass the typical feedback activation to rewire the system toward cell differentiation irrespective of growth factor identity.
Synopsis
Dynamic manipulation of ERK signaling at the single cell level reveals new features of the MAPK network topology and induces robust signaling responses that rewire cell fate decision independently of growth factor identity.
Sustained growth factor stimulation induces heterogeneous ERK dynamics, while pulsed growth factor stimulation homogenizes ERK dynamics in a cell population.
Dynamic manipulation of ERK signaling using growth factor pulses in living cells, reveals novel features of MAPK network topology and enhances previous mathematical models of MAPK signaling.
Pulsed growth factor stimulation at adequate frequencies predicted by an updated model of MAPK signaling rewires cell fate.
Graphical Abstract
Dynamic manipulation of ERK signaling at the single cell level reveals new features of the MAPK network topology and induces robust signaling responses that rewire cell fate decision independently of growth factor identity.
Publisher
Nature Publishing Group UK,EMBO Press,John Wiley and Sons Inc,Springer Nature
Subject
/ Cell Differentiation - drug effects
/ Dynamics
/ EMBO11
/ EMBO33
/ EMBO37
/ Extracellular signal-regulated kinase
/ Extracellular Signal-Regulated MAP Kinases - metabolism
/ Fluorescence Resonance Energy Transfer
/ Intercellular Signaling Peptides and Proteins - pharmacology
/ Kinases
/ Microfluidic Analytical Techniques
/ Proteins
/ Rats
