title: A force balance can explain local and global cell movements during early zebrafish development.
abstract: Embryonic morphogenesis takes place via a series of dramatic collective cell movements. The mechanisms that coordinate these intricate structural transformations across an entire organism are not well understood. In this study, we used gentle mechanical deformation of developing zebrafish embryos to probe the role of physical forces in generating long-range intercellular coordination during epiboly, the process in which the blastoderm spreads over the yolk cell. Geometric distortion of the embryo resulted in nonuniform blastoderm migration and realignment of the anterior-posterior (AP) axis, as defined by the locations at which the head and tail form, toward the new long axis of the embryo and away from the initial animal-vegetal axis defined by the starting location of the blastoderm. We found that local alterations in the rate of blastoderm migration correlated with the local geometry of the embryo. Chemical disruption of the contractile ring of actin and myosin immediately vegetal to the blastoderm margin via Ca(2+) reduction or treatment with blebbistatin restored uniform migration and eliminated AP axis reorientation in mechanically deformed embryos; it also resulted in cellular disorganization at the blastoderm margin. Our results support a model in which tension generated by the contractile actomyosin ring coordinates epiboly on both the organismal and cellular scales. Our observations likewise suggest that the AP axis is distinct from the initial animal-vegetal axis in zebrafish.
authors.affiliation: Department of Chemical Engineering, Stanford University, Stanford, California.
authors.forename: Jack
authors.initials: J
authors.lastname: Chai
authors.affiliation: Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, California.
authors.forename: Andrea L
authors.initials: AL
authors.lastname: Hamilton
authors.affiliation: Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, California.
authors.forename: Michael
authors.initials: M
authors.lastname: Krieg
authors.affiliation: Department of Chemical Engineering, Stanford University, Stanford, California.
authors.forename: Craig D
authors.initials: CD
authors.lastname: Buckley
authors.affiliation: Department of Bioengineering, Stanford University, Stanford, California.
authors.forename: Ingmar H
authors.initials: IH
authors.lastname: Riedel-Kruse
authors.affiliation: Department of Chemical Engineering, Stanford University, Stanford, California; Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, California. Electronic address: alex.dunn@stanford.edu.
authors.forename: Alexander R
authors.initials: AR
authors.lastname: Dunn
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002413:Cations, Divalent / Q000378:metabolism; D002465:Cell Movement / Q000187:drug effects / Q000502:physiology*; D003198:Computer Simulation; D005110:Extracellular Space / Q000378:metabolism; D006576:Heterocyclic Compounds, 4 or More Rings / Q000008:administration & dosage; D018613:Microscopy, Confocal; D008954:Models, Biological; D009218:Myosins / Q000378:metabolism; D010812:Physical Stimulation; D015027:Zebrafish / Q000196:embryology*
chemical_list: D000199:Actins; D002413:Cations, Divalent; D006576:Heterocyclic Compounds, 4 or More Rings; C472645:blebbistatin; D009218:Myosins; D002118:Calcium