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Updated: Jul 6, 2026
A Neonatal Mouse Spinal Cord Compression Injury Model
Published on: March 27, 2016
Mice with an anterior cleft of the palate survive neonatal lethality
Shuping Gu1, Na Wei, Xueyan Yu
1Section of Oral Biology, The Ohio State University College of Dentistry, Columbus, Ohio 43210, USA.
Abstract:
Many genes are known to function in a region-specific manner in the developing secondary palate. We have previously shown that Shox2-deficient embryos die at mid-gestation stage and develop an anterior clefting phenotype. Here, we show that mice carrying a conditional inactivation of Shox2 in the palatal mesenchyme survive the embryonic and neonatal lethality, but develop a wasting syndrome. Phenotypic analyses indicate a delayed closure of the secondary palate at the anterior end, leading to a failed fusion of the primary and secondary palates. Consistent with a role proposed for Shox2 in skeletogenesis, Shox2 inactivation causes a significantly reduced bone formation in the hard palate, probably due to a down-regulation of Runx2 and Osterix. We conclude that the secondary palatal shelves are capable of fusion with each other, but fail to fuse with the primary palate in a developmentally delayed manner. Mice carrying an anterior cleft can survive neonatal lethality.
Insights
Conditional Shox2 inactivation in mice allows survival but causes delayed anterior palate fusion and reduced bone formation. This research clarifies Shox2's role in craniofacial development and survival.
Area of Science:
- Developmental biology
- Genetics
- Skeletal biology
Background:
- Shox2 (Short stature homeobox 2) is crucial for embryonic development, with deficiency causing mid-gestation lethality and anterior clefting.
- Previous studies indicated Shox2's importance in embryonic development, but its specific role in palatal fusion and skeletogenesis remained unclear.
Purpose of the Study:
- To investigate the function of Shox2 in palatal mesenchyme during secondary palate development.
- To determine the consequences of conditional Shox2 inactivation on palatal fusion, skeletogenesis, and survival.
Main Methods:
- Conditional inactivation of the Shox2 gene in palatal mesenchyme of mice.
- Phenotypic analysis of embryonic and neonatal development, focusing on palatal fusion and skeletal structure.
- Assessment of bone formation markers, including Runx2 and Osterix expression.
Main Results:
- Conditional Shox2 inactivation enabled survival beyond mid-gestation, although mice developed a wasting syndrome.
- Delayed closure of the secondary palate at the anterior end was observed, resulting in failed fusion between the primary and secondary palates.
- Significantly reduced bone formation in the hard palate was evident, likely due to down-regulation of Runx2 and Osterix.
Conclusions:
- Shox2 is essential for the timely fusion of the secondary palate with the primary palate.
- Conditional Shox2 inactivation in palatal mesenchyme leads to impaired skeletogenesis and delayed palatal fusion, but allows for survival.
- These findings highlight Shox2's critical role in craniofacial development and bone formation.
