Significance
Cellular signaling pathways respond to a wide range of stimuli. How signaling circuits are activated without an instructive stimulus and what this is good for are less clear. Combining theoretical and experimental approaches, we show that curvature-sensing proteins stabilize stochastic membrane deformations to nucleate a self-organizing actin-regulatory signaling circuit. In neurons, these signaling hubs control the initiation of exploratory filopodia that sample the cell vicinity for appropriate synaptic partners. The extent and diversity of proteins capable of forming self-organizing circuits at stochastically deformed membranes indicates a general signaling mechanism.
All living matter is subject to continuous adaptation and functional optimization via natural selection. Consequentially, structures with close morphological resemblance repeatedly appear across the phylogenetic tree. How these designs emerge at the cellular level is not fully understood. Here, we explore core concepts of functional morphology and discuss its cause and consequences, with a specific focus on emerging properties of self-organizing systems as the potential driving force. We conclude with open questions and limitations that are present when studying shape–function interdependence in single cells and cellular ensembles.
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