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Functional expression study of igf2 antisense transcript in mouse.
Carolina Duart-Garcia1, Martin H Braunschweig2
1Institute of Genetics, Vetsuisse Faculty, University of Bern, Bremgartenstrasse 109a, 3001 Berne, Switzerland ; Graduate School for Cellular and Biomedical Sciences, Theodor Kocher Institute, University of Bern, Freiestrasse 1, 3012 Berne, Switzerland.
International Journal of Genomics
|February 20, 2014
Summary
The insulin-like growth factor antisense gene (Igf2as) is expressed in early mouse development and placenta. This study found Igf2as does not regulate Igf2, suggesting a reevaluation of the ΔDMR1-U2 knockout mouse model phenotype.
Area of Science:
- Developmental biology
- Genetics
- Molecular biology
Background:
- The role of the insulin-like growth factor antisense gene (Igf2as) in mammalian development is not fully understood.
- Previous studies linked intrauterine growth restriction in a specific mouse model to Igf2 transcription, but the involvement of Igf2as was unclear.
Purpose of the Study:
- To investigate the expression patterns of Igf2as in various mouse tissues during development.
- To determine if Igf2as interacts with or regulates Igf2 transcripts.
- To reassess the phenotype of the ΔDMR1-U2 knockout mouse model.
Main Methods:
- Analysis of Igf2as gene expression in different mouse tissues (fetal, newborn, adult liver, muscle, placenta, brain).
- Investigation of Igf2as expression in differentiating C2C12 cells.
- Examination of Igf2 expression in ΔDMR1-U2 knockout mouse placentas lacking Igf2as transcription.
Main Results:
- Igf2as expression was high in fetal and newborn liver and muscle, and also detected in placenta and brain.
- No consistent evidence of interaction between Igf2 and Igf2as transcripts was found.
- Igf2 expression in knockout placentas lacking Igf2as was comparable to wild-type, indicating Igf2as does not regulate Igf2.
Conclusions:
- Igf2as plays a role in early mouse development and placental function.
- Igf2as does not regulate Igf2 sense transcripts.
- The phenotype of the ΔDMR1-U2 knockout mouse should be reconsidered due to the functional Igf2as gene.
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