We have made a null mutation in the mouse activin beta(B) gene by dele
ting the portion of the gene encoding the proteolytic cleavage site an
d the majority of the coding region for the mature processed protein.
Mice homozygous for this mutation complete embryogenesis and are compl
etely viable. Approximately 40% of the homozygous mutant animals are b
orn with open eyes. Aside from the incompletely penetrant eye defects,
histopathological analysis has not revealed any other abnormalities i
n homozygous mutant animals. Breeding tests have shown that both male
and female homozygous mutant animals are fertile.