Chondrodysplasia and neurological abnormalities in ATF-2-deficient mice

Mice that has a germline mutation in activating transcription factor-2 (ATF-2) showed unusual actions of ATF-2 that cannot be found in the other family members of ATF/cAMP response element (CRE). Mutant mice exhibited lower postnatal viability and growth, with defective endochondral ossification at epiphyseal plates similar to human hypochondroplasia. The animals also exhibited hyperactivity, impaired hearing and ataxic gait. ATF-2-deficient mice manifested a need for skeletal and central nervous system development.