NDLI: Information Transfer in Gonadotropin-releasing Hormone (GnRH) Signaling EXTRACELLULAR SIGNAL-REGULATED KINASE (ERK)-MEDIATED FEEDBACK LOOPS CONTROL HORMONE SENSING

Content Provider	Journal of Biological Chemistry (JBC)
Author	Garner, Kathryn L. Perrett, Rebecca M. Voliotis, Margaritis Bowsher, Clive Pope, George R. Pham, Thanh Caunt, Christopher J. Tsaneva-Atanasova, Krasimira McArdle, Craig A.
Abstract	Cell signaling pathways are noisy communication channels, and statistical measures derived from information theory can be used to quantify the information they transfer. Here we use single cell signaling measures to calculate mutual information as a measure of information transfer via gonadotropin-releasing hormone (GnRH) receptors (GnRHR) to extracellular signal-regulated kinase (ERK) or nuclear factor of activated T-cells (NFAT). This revealed mutual information values <1 bit, implying that individual GnRH-responsive cells cannot unambiguously differentiate even two equally probable input concentrations. Addressing possible mechanisms for mitigation of information loss, we focused on the ERK pathway and developed a stochastic activation model incorporating negative feedback and constitutive activity. Model simulations revealed interplay between fast (min) and slow (min-h) negative feedback loops with maximal information transfer at intermediate feedback levels. Consistent with this, experiments revealed that reducing negative feedback (by expressing catalytically inactive ERK2) and increasing negative feedback (by Egr1-driven expression of dual-specificity phosphatase 5 (DUSP5)) both reduced information transfer from GnRHR to ERK. It was also reduced by blocking protein synthesis (to prevent GnRH from increasing DUSP expression) but did not differ for different GnRHRs that do or do not undergo rapid homologous desensitization. Thus, the first statistical measures of information transfer via these receptors reveals that individual cells are unreliable sensors of GnRH concentration and that this reliability is maximal at intermediate levels of ERK-mediated negative feedback but is not influenced by receptor desensitization.
Related Links	http://www.jbc.org/content/291/5/2246.abstract
Ending Page	2259
Starting Page	2246
Page Count	14
File Format	HTM / HTML PDF
ISSN	00219258
Journal	Journal of Biological Chemistry (JBC)
Issue Number	5
Volume Number	291
DOI	10.1074/jbc.M115.686964
e-ISSN	1083351X
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2016-01-29
Access Restriction	Open
Subject Keyword	Cell signaling Extracellular signal-regulated kinase (ERK) G protein-coupled receptor (GPCR) Mathematical modeling Mitogen-activated protein kinase (MAPK) Gonadotropin-releasing hormone Mutual information Signal transduction Computational Biology
Alternative Title	Information Transfer in Gonadotropin-releasing Hormone (GnRH) Signaling
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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Information Transfer in Gonadotropin-releasing Hormone (GnRH) Signaling

Role of Dynamin, Src, and Ras in the Protein Kinase C-mediated Activation of ERK by Gonadotropin-releasing Hormone

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Information Transfer in Gonadotropin-releasing Hormone (GnRH) Signaling EXTRACELLULAR SIGNAL-REGULATED KINASE (ERK)-MEDIATED FEEDBACK LOOPS CONTROL HORMONE SENSING

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