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Three and Four-Dimensional Visualization and Analysis Approaches to Study Vertebrate Axial Elongation and Segmentation

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Tgif1 and Tgif2 Regulate Axial Patterning in Mouse.

Tiffany A Melhuish¹, Kenichiro Taniguchi¹, David Wotton¹

¹Department of Biochemistry and Molecular Genetics, and Center for Cell Signaling, University of Virginia, Charlottesville, United States of America.

|May 18, 2016

Summary

This summary is machine-generated.

Loss of Tgif1 alone in mice causes axial patterning defects and posterior transformations. Combined Tgif1 and Tgif2 loss exacerbates these defects, indicating TGIF proteins regulate embryonic development.

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Area of Science:

Developmental Biology
Genetics
Molecular Biology

Background:

TGIF1 and TGIF2 are transcriptional repressors inhibiting TGF-β signaling.
TGIF1 mutations are linked to holoprosencephaly (HPE) in humans.
Tgif1/Tgif2 double knockout mouse embryos exhibit severe developmental failures.

Purpose of the Study:

Investigate the role of Tgif1 in mouse axial patterning.
Determine the combined effects of Tgif1 and Tgif2 loss on embryonic development.
Assess the impact of retinoic acid on Tgif1 mutant phenotypes.

Main Methods:

Analysis of Tgif1 null mutant mice on a C57BL/6 background.
Examination of axial patterning and Hoxc6 expression.
Assessment of Tgif1/Tgif2 double null and retinoic acid-treated embryos.

Main Results:

Tgif1 loss alone causes defective axial patterning, including posterior transformation (extra C7 ribs) and cervical vertebrae defects (C1-C5).
Combined Tgif1/Tgif2 mutations enhance the severity and penetrance of these phenotypes.
Retinoic acid exposure amplifies Tgif1-associated developmental defects.

Conclusions:

TGIF1 and TGIF2 are crucial regulators of axial patterning in mouse development.
Reduced TGIF function sensitizes embryos to teratogenic effects of retinoic acid.
These findings provide insights into the genetic basis of developmental abnormalities like HPE.