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A Dual Receptor Crosstalk Model of G-Protein-Coupled Signal Transduction 1 2 3 4 4 Patrick Flaherty , Mala L. Radhakrishnan , Tuan Dinh , Robert A. Rebres , Tamara I. Roach , Michael I. Jordan5, Adam P. Arkin6,7,8* 1 Department of Electrical Engineering and Computer Sciences, University of California Berkeley, Berkeley, California, United States of America, 2 Computer Science and Artificial Intelligence Laboratory, Department of Chemistry, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America, 3 Department of Bioengineering, University of California Berkeley, Berkeley, California, United States of America, 4 Alliance for Cellular Signaling, Northern California Institute for Research and Education and the University of California, Veterans Affairs Medical Center, San Francisco, California, United States of America, 5 Department of Statistics and Computer Science Division, University of California Berkeley, Berkeley, California, United States of America, 6 Physical Biosciences Division, Lawrence Berkeley Laboratory, Berkeley, California, United States of America, 7 Howard Hughes Medical Institute, University of California Berkeley, Berkeley, California, United States of America, 8 Department of Bioengineering, University of California Berkeley, Berkeley, California, United States of America Abstract Macrophage cells that are stimulated by two different ligands that bind to G-protein-coupled receptors (GPCRs) usually respond as if the stimulus effects are additive, but for a minority of ligand combinations the response is synergistic. The G- protein-coupled receptor system integrates signaling cues from the environment to actuate cell morphology, gene expre