PUBLICATION

Leading and trailing cells cooperate in collective migration of the zebrafish Posterior Lateral Line primordium

Authors
Dalle Nogare, D., Somers, K., Rao, S., Matsuda, M., Reichman-Fried, M., Raz, E., Chitnis, A.B.
ID
ZDB-PUB-140728-4
Date
2014
Source
Development (Cambridge, England)   141(16): 3188-96 (Journal)
Registered Authors
Chitnis, Ajay, Raz, Erez, Reichman-Fried, Michal
Keywords
none
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Cell Communication
  • Cell Movement
  • Chemokine CXCL12/physiology
  • Chemokines/metabolism
  • Computer Simulation
  • Fibroblast Growth Factors/metabolism
  • Gene Expression Regulation, Developmental*
  • Lateral Line System/embryology*
  • Receptors, CXCR/physiology
  • Receptors, CXCR4/physiology
  • Signal Transduction
  • Zebrafish/embryology*
  • Zebrafish Proteins/physiology
PubMed
25063456 Full text @ Development
Abstract
Collective migration of cells in the zebrafish Posterior Lateral Line primordium (PLLp) along a path defined by Cxcl12a expression depends on Cxcr4b receptors in leading cells and on Cxcr7b in trailing cells. Cxcr7b-mediated degradation of Cxcl12a by trailing cells generates a local gradient of Cxcl12a that guides PLLp migration. Agent-based computer models were built to explore how a polarized response to Cxcl12a, mediated by Cxcr4b in leading cells and prevented by Cxcr7b in trailing cells, determines unidirectional migration of the PLLp. These chemokine signaling-based models effectively recapitulate many behaviors of the PLLp and provide potential explanations for the characteristic behaviors that emerge when the PLLp is severed by laser to generate leading and trailing fragments. As predicted by our models, the bilateral stretching of the leading fragment is lost when chemokine signaling is blocked in the PLLp. However, movement of the trailing fragment toward the leading cells, which was also thought to be chemokine dependent, persists. This suggested that a chemokine-independent mechanism, not accounted for in our models, is responsible for this behavior. Further investigation of trailing cell behavior shows that their movement toward leading cells depends on FGF signaling and it can be re-oriented by exogenous FGF sources. Together, our observations reveal the simple yet elegant manner in which leading and trailing cells coordinate migration; while leading cells steer PLLp migration by following chemokine cues, cells further back play follow-the-leader as they migrate toward FGFs produced by leading cells.
Genes / Markers
Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes