PUBLICATION
Extra-embryonic syndecan 2 regulates organ primordia migration and fibrillogenesis throughout the zebrafish embryo
- Authors
- Arrington, C.B., and Yost, H.J.
- ID
- ZDB-PUB-090828-15
- Date
- 2009
- Source
- Development (Cambridge, England) 136(18): 3143-3152 (Journal)
- Registered Authors
- Yost, H. Joseph
- Keywords
- Cardiac, Fibronectin, Gut, Heart, Proteoglycan, Syndecan, Zebrafish
- MeSH Terms
-
- Animals
- Cell Lineage
- Cell Movement/physiology*
- Cell Polarity
- Egg Yolk/metabolism
- Embryo, Nonmammalian/anatomy & histology
- Embryo, Nonmammalian/physiology
- Endocardium/cytology
- Endocardium/metabolism
- Endoderm/cytology
- Endoderm/metabolism
- Gene Knockdown Techniques
- Membrane Proteins/genetics
- Membrane Proteins/metabolism
- Morphogenesis/physiology*
- Myocytes, Cardiac/cytology
- Myocytes, Cardiac/metabolism
- Syndecan-2/genetics
- Syndecan-2/metabolism*
- Zebrafish*/anatomy & histology
- Zebrafish*/embryology
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 19700618 Full text @ Development
Citation
Arrington, C.B., and Yost, H.J. (2009) Extra-embryonic syndecan 2 regulates organ primordia migration and fibrillogenesis throughout the zebrafish embryo. Development (Cambridge, England). 136(18):3143-3152.
Abstract
One of the first steps in zebrafish heart and gut organogenesis is the migration of bilateral primordia to the midline to form cardiac and gut tubes. The mechanisms that regulate this process are poorly understood. Here we show that the proteoglycan syndecan 2 (Sdc2) expressed in the extra-embryonic yolk syncytial layer (YSL) acts locally at the YSL-embryo interface to direct organ primordia migration, and is required for fibronectin and laminin matrix assembly throughout the embryo. Surprisingly, neither endogenous nor exogenous sdc2 expressed in embryonic cells can compensate for knockdown of sdc2 in the YSL, indicating that Sdc2 expressed in extra-embryonic tissues is functionally distinct from Sdc2 in embryonic cells. The effects of sdc2 knockdown in the YSL can be rescued by extra-embryonic Sdc2 lacking an extracellular proteolytic cleavage (shedding) site, but not by extra-embryonic Sdc2 lacking extracellular glycosaminoglycan (GAG) addition sites, suggesting that distinct GAG chains on extra-embryonic Sdc2 regulate extracellular matrix assembly, cell migration and epithelial morphogenesis of multiple organ systems throughout the embryo.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping