PUBLICATION
Muscle development is disrupted in zebrafish embryos deficient for fibronectin
- Authors
- Snow, C.J., Peterson, M.T., Khalil, A., and Henry, C.A.
- ID
- ZDB-PUB-080902-14
- Date
- 2008
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 237(9): 2542-2553 (Journal)
- Registered Authors
- Henry, Clarissa A.
- Keywords
- Fibronectin, somite, muscle, zebrafish, morphogenesis, 2D wavelet transform modulus maxima, aei/deltaD, myofiber, MTJ
- MeSH Terms
-
- In Situ Hybridization
- Gene Expression Regulation, Developmental
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- Models, Biological
- Animals
- Muscle Fibers, Slow-Twitch/metabolism
- Muscle Fibers, Fast-Twitch/metabolism
- Embryo, Nonmammalian/embryology
- Embryo, Nonmammalian/metabolism
- Immunohistochemistry
- Muscle Development/genetics
- Muscle Development/physiology*
- Zebrafish/embryology
- Zebrafish/metabolism*
- Somites/embryology
- Somites/metabolism
- Fibronectins/genetics
- Fibronectins/metabolism*
- PubMed
- 18729220 Full text @ Dev. Dyn.
Citation
Snow, C.J., Peterson, M.T., Khalil, A., and Henry, C.A. (2008) Muscle development is disrupted in zebrafish embryos deficient for fibronectin. Developmental Dynamics : an official publication of the American Association of Anatomists. 237(9):2542-2553.
Abstract
After somitogenesis, skeletal muscle precursors elongate into muscle fibers that anchor to the somite boundary, which becomes the myotome boundary. Fibronectin (Fn) is a major component of the extracellular matrix in both boundaries. Although Fn is required for somitogenesis, effects of Fn disruption on subsequent muscle development are unknown. We show that fn knockdown disrupts myogenesis. Muscle morphogenesis is more disrupted in fn morphants than in a mutant where initial somite boundaries did not form, aei/deltaD. We quantified this disruption using the two-dimensional Wavelet-Transform Modulus Maxima method, which uses the variation of intensity in an image with respect to the direction considered to characterize the structure in a cell lattice. We show that fibers in fn morphants are less organized than in aei/deltaD mutant embryos. Fast- and slow-twitch muscle lengths are also more frequently uncoupled. These data suggest that fn may function to regulate fiber organization and limit fast-twitch muscle fiber length.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping