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Mesodermal development in mouse embryos mutant for fibronectin
E N Georges-Labouesse1, E L George, H Rayburn
1Howard Hughes Medical Institute, Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139, USA.
Abstract:
Three independent mutations were made by homologous recombination in two different regions of the fibronectin (FN) gene; all three appeared to be functional null mutations. The embryonic lethal phenotypes of these mutations were indistinguishable; all three FN mutant strains show mesodermal defects and fail to develop notochord or somites. Nevertheless analysis with lineage markers (Brachyury, sonic hedgehog, Notch-1, and mox-1) showed that both the notochord and the somite lineages were induced at the correct times and places. Furthermore, notochord precursor cells showed extensive cell migration in the absence of FN. However, neither notochord nor somites condensed properly in the absence of FN. These results show that specification of notochordal and somitic mesodermal lineages and significant cell migration are independent of fibronectin but that correct morphogenesis of these structures is FN-dependent.
Insights
Fibronectin (FN) is essential for proper mesodermal development in embryos. While FN is not required for notochord and somite cell specification or migration, it is crucial for their morphogenesis.
Area of Science:
- Developmental Biology
- Molecular Biology
- Genetics
Background:
- Fibronectin (FN) is a crucial extracellular matrix protein involved in cell adhesion, migration, and differentiation.
- Understanding the specific roles of FN in early embryonic development is vital for comprehending developmental processes.
Purpose of the Study:
- To investigate the necessity of fibronectin for the specification, migration, and morphogenesis of mesodermal structures, specifically the notochord and somites.
- To elucidate the functional independence of mesodermal lineage induction and cell migration from fibronectin.
Main Methods:
- Generation of three independent fibronectin (FN) gene knockout mutations using homologous recombination.
- Analysis of embryonic lethal phenotypes in FN mutant strains.
- Utilizing lineage markers (Brachyury, sonic hedgehog, Notch-1, mox-1) to track cell fate and induction.
- Observing notochord precursor cell migration and tissue condensation in wild-type and FN-deficient embryos.
Main Results:
- All three FN null mutations resulted in indistinguishable embryonic lethal phenotypes, characterized by mesodermal defects and failure to develop notochord or somites.
- Lineage marker analysis confirmed that notochord and somite lineages were induced correctly in time and place, even without functional FN.
- Notochord precursor cells exhibited significant migration in the absence of FN.
- However, proper condensation of both notochord and somites was impaired in FN-deficient embryos.
Conclusions:
- Mesodermal lineage specification and substantial cell migration during embryogenesis are independent of fibronectin.
- Fibronectin is essential for the correct morphogenesis, specifically the condensation, of the notochord and somites.
- These findings highlight distinct roles for FN in early embryonic development, separating lineage determination from tissue formation.
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