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Tenascin-C in peripheral nerve morphogenesis
1Department of Biophysical Chemistry, Biocenter of the University, Basel, Switzerland.
Perspectives on Developmental Neurobiology
|January 1, 1994
Summary
Tenascin-C (TN-C), an extracellular matrix molecule, promotes neurite outgrowth in developing neurons but inhibits satellite cell migration. Its function appears redundant in mice, suggesting other molecules compensate for TN-C
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- Extracellular matrix (ECM) molecule tenascin/cytotactin (TN-C) is highly expressed by glial precursor cells in developing chick embryo peripheral nerves.
- TN-C mRNA synthesis peaks during maximal axonal growth periods.
Purpose of the Study:
- Investigate the role of TN-C in neurite outgrowth and satellite cell behavior during peripheral nerve development.
- Identify TN-C domains responsible for mediating neuronal and glial cell interactions.
Main Methods:
- In vitro studies using TN-C as a substrate for chick embryo motor and sensory neurons.
- Assessing neurite outgrowth and satellite cell attachment/migration on TN-C and other ECM molecules.
- Utilizing antibodies against beta 1 integrins to investigate receptor involvement.
Main Results:
- TN-C promotes neurite outgrowth in motor and sensory neurons, with activity being developmentally regulated.
- A C-terminal TN-C domain mediates neurite outgrowth, involving integrin receptors.
- TN-C inhibits satellite cell migration while allowing attachment, acting as a barrier against other ECMs.
Conclusions:
- TN-C exhibits dual action: promoting neuronal growth and inhibiting glial cell migration.
- The repulsive effect on satellite cells is likely mediated by additional TN-C domains.
- TN-C's role may be redundant in mice, with its functions potentially compensated by other molecules.