Knockout of the mouse activin beta A gene (Matzuk et al, 1995,Ferguson et al, 1998) prevents the formation of dimers called activin A, activin AB and inhibin A. While the heterozygotes are viable, the homozygous appeared to be healthy at birth but die postnatally after 24 hours. The developmental defects include the lack of whiskers, incisors and lower molars causing the secondary abnormality of the alveolar ridge. The homozygous mice also had defects in their secondary palate or lack or immature hard palate causing cleft palate and preventing suckling. However, the maxillary molars develop normally.
Knockout of another gene, activin beta B, prevents the formation of dimers called activin B, activin AB and inhibin B. In this case the homozygous mice are viable but have open eyelids perinatally and defective female reproduction. Double knockouts of both activin beta A and B have a phenotype that is a combination of the individual knockouts. This shows that in mouse there is no redundancy between these proteins during development, i.e. the lack of other cannot be compensated by the presence of another. In mouse the zygotic expression of activins is neither essential for mesoderm formation.
|Jackson Mouse Genome Database||Transgene Database||OMIM|