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Caudal dysgenesis in Islet-1 transgenic mice
Yunhua Li Muller1, Yir Gloria Yueh, Paul J Yaworsky
1Samuel C. Johnson Medical Research Center, Mayo Clinic Scottsdale, Scottsdale, Arizona, USA.
Summary
Maternal diabetes causes birth defects. Mice with altered Isl-1 gene show severe tail growth issues, suggesting pancreatic genes may cause these developmental problems.
Area of Science:
- Developmental biology
- Genetics
- Endocrinology
Background:
- Maternal diabetes during pregnancy can lead to diabetic embryopathy, a range of birth defects.
- These defects include heart abnormalities, neural tube defects, and caudal dysgenesis syndromes.
Purpose of the Study:
- To investigate the role of the homeodomain transcription factor Isl-1 in the development of caudal growth defects.
- To explore the link between pancreatic transcription factors and birth defects associated with diabetes.
Main Methods:
- Generation of mice transgenic for the homeodomain transcription factor Isl-1.
- Analysis of caudal growth defects in transgenic mice.
- Comparison with findings from mutations in the pancreatic transcription factor HLXB9.
Main Results:
- Transgenic mice for Isl-1 exhibited profound caudal growth defects, mimicking human sacral/caudal agenesis.
- Aberrant regulation of Isl-1 led to increased mesodermal cell death.
- The severity of defects correlated with transgene dosage.
Conclusions:
- The homeodomain transcription factor Isl-1 plays a critical role in caudal development.
- Dysregulation of pancreatic transcription factors, like Isl-1, is implicated in the pathogenesis of diabetic embryopathy.
- These findings highlight a potential mechanism linking maternal diabetes to specific birth defects.
