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Effects of the TWis mutation on notochord formation and mesodermal patterning
F L Conlon1, C V Wright, E J Robertson
1Department of Molecular Biology, Harvard University, Cambridge, MA 02138, USA.
Mechanisms of Development
|February 1, 1995
Summary
The mouse T (Brachyury) gene is crucial for mesodermal patterning. Mutations cause notochord defects, impacting somite development and leading to midgestation lethality in homozygous mutants.
Area of Science:
- Developmental Biology
- Genetics
- Molecular Biology
Background:
- The mouse T (Brachyury) gene plays a vital role in early mesodermal patterning.
- Mutations in T lead to midgestation lethality and defects in mesodermal tissues like the notochord and somites.
Purpose of the Study:
- To investigate the function of the T gene in patterning somitic and posterior mesoderm along the anterior-posterior axis.
- To analyze the spatial relationships and differentiation of mesodermal populations in T mutant mice.
Main Methods:
- Utilized whole-mount antibody double labeling techniques.
- Examined the expression of molecular markers (sonic hedgehog/vertebrate homolog of hedgehog 1 (Shh/vhh-1), goosecoid, mox-1, cdx-4, twist) in wild-type and TWis mutant mice.
Main Results:
- TWis homozygous mutants form notochordal precursor cells but fail to proliferate or differentiate.
- Aberrant somitic differentiation observed, indicated by mox-1 protein and twist RNA expression.
- Twist expression in paraxial mesoderm is T-dependent, while Shh/vhh-1, goosecoid, mox-1, and cdx-4 are not.
Conclusions:
- T gene is essential for notochordal tissue maintenance.
- T-dependent signals are required for subsequent somite differentiation.
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