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Morphological features of tail bud development in truncate mouse mutants
Dinko Mitrecić1, Ljiljana Kostović-Knezević, Srećko Gajović
1Croatian Institute for Brain Research, School of Medicine, University of Zagreb, Zagreb, Croatia.
Cells, Tissues, Organs
|November 20, 2004
Summary
The truncate (tc) mutation in mice disrupts tail bud development, causing notochord malformations. This study reveals improper tail bud regionalization, linking neural tube and tail gut, leading to notochord defects in truncate mutants.
Area of Science:
- Developmental Biology
- Genetics
- Morphology
Background:
- The truncate (tc) mutation in mice is associated with a partial absence of the notochord in the embryonic tail.
- Understanding the genetic basis of notochord development is crucial for comprehending embryonic patterning.
Purpose of the Study:
- To investigate the effect of the truncate (tc) mutation on tail bud development.
- To analyze the morphological consequences of the tc mutation on notochord and associated structures.
Main Methods:
- Serial semithin sectioning of homozygous truncate mutant and wild-type mouse embryos.
- Comparative morphological analysis of tail bud structures, including the notochord, neural tube, and gut.
Main Results:
- In truncate mutants, the tail cord failed to connect with the notochord, instead connecting to an additional lumen of the tail gut, causing duplication.
- The notochord in truncate embryos was fragmented and often associated with the ventral border of the secondary neural tube.
- Wild-type embryos exhibited a continuous connection between the tail bud, medullary cord, secondary neural tube, tail cord, notochord, and gut.
Conclusions:
- The truncate mutation leads to improper regionalization of the tail bud.
- Aberrant association of the notochord with the neural tube instead of the tail gut is implicated in the segmental notochordal defects observed in truncate mutants.