Segmental assembly of fibronectin matrix requires rap1b and integrin alpha5
- Authors
- Lackner, S., Schwendinger-Schreck, J., Jülich, D., and Holley, S.A.
- ID
- ZDB-PUB-121206-14
- Date
- 2013
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 242(2): 122-131 (Journal)
- Registered Authors
- Jülich, Dörthe
- Keywords
- Rap1, GTPase, integrin, fibronectin, somitogenesis, zebrafish
- MeSH Terms
-
- Animals
- Cell Polarity/physiology
- Cleavage Stage, Ovum/physiology*
- Extracellular Matrix/metabolism*
- Fibronectins/metabolism*
- Gene Knockdown Techniques
- Image Processing, Computer-Assisted
- Immunohistochemistry
- In Situ Hybridization
- Integrin alpha5/genetics
- Integrin alpha5/metabolism*
- Microscopy, Fluorescence
- Morphogenesis/physiology
- Morpholinos/genetics
- Signal Transduction/physiology*
- Somites/embryology
- Zebrafish/embryology*
- Zebrafish Proteins/metabolism*
- rap GTP-Binding Proteins/genetics
- rap GTP-Binding Proteins/metabolism*
- PubMed
- 23192979 Full text @ Dev. Dyn.
Background:
During segmentation of the zebrafish embryo, inside-out signaling activates Integrin α5, which is necessary for somite border morphogenesis. The direct activator of Integrin α5 during this process is unknown. One candidate is Rap1b, a small monomeric GTPase implicated in Integrin activation in the immune system.
Results:
Knockdown of rap1b, or overexpression of a dominant negative rap1b, causes a mild axis elongation defect in zebrafish. However, disruption of rap1b function in integrin α5-/- mutants results in a strong reduction in Fibronectin (FN) matrix assembly in the paraxial mesoderm and a failure in somite border morphogenesis along the entire anterior-posterior axis. Somite patterning appears unaffected, as her1 oscillations are maintained in single and double morphants/mutants, but somite polarity is gradually lost in itgα5-/-; rap1b MO embryos.
Conclusions:
In itgα5-/- mutants, rap1b is required for proper somite border morphogenesis in zebrafish. The loss of somite borders is not a result of aberrant segmental patterning. Rather, somite boundary formation initiates but is not completed, due to the failure to assemble FN matrix along the nascent boundary. We propose a model in which Rap1b activates Integrin/Fibronectin receptors as part of an “inside-out” signaling pathway that promotes Integrin binding to FN, FN matrix assembly and subsequent stabilization of morphological somite boundaries.