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Retinoic acid receptor beta 2 (RAR beta 2) null mutant mice appear normal
C Mendelsohn1, M Mark, P Dollé
1Laboratoire de Génétique Moléculaire des Eucaryotes du CNRS, Institut de Chimie Biologique, Faculté de Médecine, Strasbourg, France.
Developmental Biology
|November 1, 1994
Summary
Retinoic acid (RA) is crucial for development, but excess can cause birth defects. This study found that the RAR beta 2 isoform is not essential for normal development or mediating RA-induced malformations.
Area of Science:
- Developmental Biology
- Molecular Endocrinology
- Genetics
Background:
- Vertebrates are sensitive to retinoic acid (RA) levels during development.
- Nuclear receptors, including retinoic acid receptors (RARs), mediate RA signaling.
- RAR beta 2 is an abundant RAR isoform with restricted embryonic expression, potentially involved in RA teratogenicity.
Purpose of the Study:
- To investigate the role of the RAR beta 2 isoform in embryonic development.
- To determine if RAR beta 2 mediates retinoic acid-induced teratogenic effects.
Main Methods:
- Targeted gene disruption to create RAR beta 2 null mutant mice.
- Phenotypic analysis of RAR beta 2 null mutants.
- Exposure of RAR beta 2 null embryos to teratogenic doses of retinoic acid.
Main Results:
- RAR beta 2 null mutants display normal prenatal and postnatal development.
- Other RARs appear to compensate for the absence of RAR beta 2.
- RAR beta 2 is not required for mediating RA-induced malformations in developing embryos.
Conclusions:
- The RAR beta 2 isoform is dispensable for normal vertebrate development.
- RAR beta 2 does not play a critical role in mediating the teratogenic effects of excess retinoic acid.
- Redundancy in RAR signaling pathways allows for developmental compensation.