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Normal lung development in RAIG1-deficient mice despite unique lung epithelium-specific expression
Jingsong Xu1, Jun Tian, Steven D Shapiro
1Harvard Medical School, Brigham and Women's Hospital, 75 Francis St., Boston, MA 02115, USA. jxu@rics.bwh.harvard.edu
American Journal of Respiratory Cell and Molecular Biology
|January 29, 2005
Summary
RAIG1, a lung-specific orphan receptor, was studied for its role in lung development. Despite abundant expression, its inactivation did not cause developmental defects, suggesting potential functional redundancy with RAIG3.
Area of Science:
- Molecular Biology
- Developmental Biology
- Genetics
Background:
- RAIG1, 2, and 3, along with GPCR5d, form a novel subfamily of orphan G protein-coupled receptors.
- RAIG1 exhibits abundant and specific expression in the mouse lung during both development and adulthood.
- Its expression pattern and link to retinoic acid signaling suggested a role in epithelial cell differentiation during lung development.
Purpose of the Study:
- To investigate the function of RAIG1 in lung development.
- To track the spatial expression of endogenous RAIG1.
- To determine if RAIG1 plays a role in epithelial cell differentiation.
Main Methods:
- Generation of a null allele for Raig1 by "knocking-in" the lacZ gene.
- Analysis of RAIG1 expression patterns using lacZ reporter.
- Phenotypic analysis of Raig1 null mutant mice, including lung structure and epithelial cell differentiation.
Main Results:
- RAIG1 expression was observed in both proximal and distal epithelium during embryogenesis, becoming restricted to type I and type II pneumocytes and distal bronchiolar cells in postnatal lungs.
- This represents a unique epithelial cell expression pattern not previously described.
- Targeted inactivation of Raig1 did not result in significant developmental defects, with normal epithelial cell differentiation and lung structure.
Conclusions:
- Despite its specific and abundant lung expression, RAIG1 does not appear to be essential for lung development or epithelial differentiation in mice.
- Overlapping embryonic expression of RAIG3 mRNA suggests a potential for functional redundancy within the RAIG family, which may compensate for the loss of RAIG1.