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Exogenous tenascin inhibits mesodermal cell migration during amphibian gastrulation
1Laboratoire de Biologie Expérimentale, U.A. 1135 CNRS, Université Pierre et Marie Curie, Paris, France.
Developmental Biology
|February 1, 1990
Summary
Tenascin, an extracellular matrix glycoprotein, inhibits mesodermal cell migration during amphibian gastrulation. This interference with cell-matrix interactions can be reversed by a specific antibody, suggesting tenascin
Area of Science:
- Developmental Biology
- Cell Biology
- Extracellular Matrix Research
Background:
- Amphibian gastrulation is a crucial developmental process involving extensive cell migration.
- The extracellular matrix (ECM) plays a vital role in guiding cell movements during embryonic development.
- Tenascin is an ECM glycoprotein whose function in early vertebrate development is not fully understood.
Purpose of the Study:
- To investigate the role of tenascin in regulating mesodermal cell migration during amphibian gastrulation.
- To determine how tenascin affects cell-ECM interactions in vivo and in vitro.
- To identify potential mechanisms for tenascin's influence on cell migration.
Main Methods:
- In vitro assays using isolated dorsal marginal zone (DMZ) cells and DMZ explants on fibronectin or gastrula ECM substrata.
- Microinjection of tenascin into the blastocoel cavity of amphibian embryos at different developmental stages.
- Scanning electron microscopy to examine cell migration in arrested gastrulae.
- In vitro and in vivo rescue experiments using a monoclonal antibody (mAb Tn68).
- Analysis of tenascin binding to ECM fibrils post-injection.
Main Results:
- Exogenous tenascin inhibited mesodermal cell spreading and migration in vitro.
- Microinjection of tenascin into embryos led to gastrulation arrest in over 80% of cases, with blocked mesodermal cell migration.
- Tenascin inhibited cell migration even after cells had contacted the ECM.
- The inhibitory effects of tenascin were reversible in vitro and in vivo using mAb Tn68.
- Injected tenascin rapidly bound to embryonic ECM fibrils.
Conclusions:
- Exogenous tenascin can be incorporated into the embryonic ECM and disrupts mesodermal cell migration in vivo.
- Tenascin interferes with essential cell-matrix interactions, particularly with fibronectin-rich matrices, during gastrulation.
- Targeting specific binding sites on tenascin can restore normal cell migration, highlighting its functional significance.