No abstract

Coupled oscillators are shown to experience two structurally different oscillation quenching types: amplitude death (AD) and oscillation death (OD). We demonstrate that both AD and OD can occur in one system and find that the transition between them underlies a classical, Turing-type bifurcation, providing a clear classification of these significantly different dynamical regimes. The implications of obtaining a homogeneous (AD) or inhomogeneous (OD) steady state, as well as their significance for physical and biological applications and control studies, are also pointed out.

SummaryThe proto-oncogenic epidermal growth factor receptor (EGFR) is a tyrosine kinase whose sensitivity to growth factors and signal duration determines cellular behavior. We resolve how EGFR's response to epidermal growth factor (EGF) originates from dynamically established recursive interactions with spatially organized protein tyrosine phosphatases (PTPs). Reciprocal genetic PTP perturbations enabled identification of receptor-like PTPRG/J at the plasma membrane and ER-associated PTPN2 as the major EGFR dephosphorylating activities. Imaging spatial-temporal PTP reactivity revealed that vesicular trafficking establishes a spatially distributed negative feedback with PTPN2 that determines signal duration. On the other hand, single-cell dose-response analysis uncovered a reactive oxygen species-mediated toggle switch between autocatalytically activated monomeric EGFR and the tumor suppressor PTPRG that governs EGFR's sensitivity to EGF. Vesicular recycling of monomeric EGFR unifies the interactions with these PTPs on distinct membrane systems, dynamically generating a network architecture that can sense and respond to time-varying growth factor signals.