ERK reinforces actin polymerization to power persistent edge protrusion during motility.
作者： Michelle C. Mendoza , Marco Vilela , Jesus E. Juarez , John Blenis , Gaudenz Danuser
DOI: 10.1126/SCISIGNAL.AAA8859
关键词:
摘要: Cells move through perpetual protrusion and retraction cycles at the leading edge. These are coordinated with substrate adhesion of cell rear. We tracked spatial temporal fluctuations in molecular activities individual moving cells to elucidate how extracellular signal–regulated kinase (ERK) signaling controlled dynamics cycles. ERK is activated by many surface receptors, we found that specifically reinforced cellular protrusions so they translated into rapid, sustained forward motion Using quantitative fluorescent speckle microscopy cross-correlation analysis, showed rate timing actin polymerization promoting recruitment nucleator Arp2/3 findings support a model which surges activity induced cues enhance Arp2/3-mediated generate power phases enough force counteract increasing membrane tension promote motility.
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