PUBLICATION

Dynamic Buffering of Extracellular Chemokine by a Dedicated Scavenger Pathway Enables Robust Adaptation during Directed Tissue Migration

Authors
Wong, M., Newton, L.R., Hartmann, J., Hennrich, M.L., Wachsmuth, M., Ronchi, P., Guzmán-Herrera, A., Schwab, Y., Gavin, A.C., Gilmour, D.
ID
ZDB-PUB-200216-10
Date
2020
Source
Developmental Cell   52(4): 492-508.e10 (Journal)
Registered Authors
Gilmour, Darren
Keywords
GPCR, adaptation, cell migration, chemokine, live imaging, membrane trafficking, robustness, self-generated gradients, zebrafish
MeSH Terms
  • Animals
  • Cell Communication
  • Cell Movement*
  • Chemokines/genetics
  • Chemokines/metabolism*
  • Embryo, Nonmammalian/cytology
  • Embryo, Nonmammalian/metabolism*
  • Phosphorylation
  • Receptors, CXCR/genetics
  • Receptors, CXCR/metabolism*
  • Receptors, CXCR4/genetics
  • Receptors, CXCR4/metabolism*
  • Signal Transduction
  • Zebrafish/genetics
  • Zebrafish/growth & development
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
32059773 Full text @ Dev. Cell
Abstract
How tissues migrate robustly through changing guidance landscapes is poorly understood. Here, quantitative imaging is combined with inducible perturbation experiments to investigate the mechanisms that ensure robust tissue migration in vivo. We show that tissues exposed to acute "chemokine floods" halt transiently before they perfectly adapt, i.e., return to the baseline migration behavior in the continued presence of elevated chemokine levels. A chemokine-triggered phosphorylation of the atypical chemokine receptor Cxcr7b reroutes it from constitutive ubiquitination-regulated degradation to plasma membrane recycling, thus coupling scavenging capacity to extracellular chemokine levels. Finally, tissues expressing phosphorylation-deficient Cxcr7b migrate normally in the presence of physiological chemokine levels but show delayed recovery when challenged with elevated chemokine concentrations. This work establishes that adaptation to chemokine fluctuations can be "outsourced" from canonical GPCR signaling to an autonomously acting scavenger receptor that both senses and dynamically buffers chemokine levels to increase the robustness of tissue migration.
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