Tissue Morphogenesis and Vascular Stability Require the Frem2 Protein, Product of the Mouse Myelencephalic Blebs Gene

Adhesive properties of cells undergoing morphogenetic rearrangements can be regulated either at the cellular level or by altering the environment in which rearrangements occur. Here, we describe the identification of a mutation (myF11) in the mouse extracellular matrix component Frem2, and provide e...

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Published inProceedings of the National Academy of Sciences - PNAS Vol. 102; no. 33; pp. 11746 - 11750
Main Authors Timmer, John R., Mak, Tracy W., Manova, Katia, Anderson, Kathryn V., Niswander, Lee
Format Journal Article
LanguageEnglish
Published United States National Academy of Sciences 16.08.2005
National Acad Sciences
Subjects
Animals
Biological Sciences
Cell adhesion & migration
Choroid plexus
Embryos
Endothelial cells
Extracellular Matrix Proteins - genetics
Extracellular Matrix Proteins - metabolism
Extremities - embryology
Gene expression
Gene Expression Regulation, Developmental
Genetic mutation
Hemorrhage
Hemorrhage - embryology
Hemorrhage - metabolism
Hemorrhage - pathology
Lungs
Medulla Oblongata - blood supply
Medulla Oblongata - embryology
Medulla Oblongata - metabolism
Mice
Morphogenesis
Mutation
Mutation - genetics
Nerve tissue
Neurons
Phenotype
Phenotypes
Rodents
Tissues
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Summary:Adhesive properties of cells undergoing morphogenetic rearrangements can be regulated either at the cellular level or by altering the environment in which rearrangements occur. Here, we describe the identification of a mutation (myF11) in the mouse extracellular matrix component Frem2, and provide evidence that suggests Frem2 expression creates an environment conducive to morphogenetic events. Loss of Frem2 function results in defects in developmental events associated with morphogenetic rearrangements of the vasculature and of tissues arising from all germ layers. The Frem2 transcript is restricted both spatially and temporally and appears in advance of cell rearrangement events. Thus, expression of Frem2 may dynamically alter the extracellular matrix to provide a substrate for cell migration and rearrangements during embryogenesis.
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Present address: Cell and Developmental Biology Department, The Weill Medical College of Cornell University, New York, NY 10021.
Author contributions: J.R.T., K.V.A., and L.N. designed research; J.R.T., T.W.M., and K.M. performed research; J.R.T., K.V.A., and L.N. analyzed data; and J.R.T., K.V.A., and L.N. wrote the paper.
Present address: Howard Hughes Medical Institute, Department of Pediatrics, University of Colorado Health Sciences Center, Aurora, CO 80045-0511.
Contributed by Kathryn V. Anderson, June 29, 2005
To whom correspondence should be addressed. E-mail: lee.niswander@uchsc.edu.
Abbreviations: E, embryonic day; ECM, extracellular matrix.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.0505404102