Table 4. Evidence that RXRα and RAR act synergistically in embryonic development.

Similar congenital defects absent (or very rare) in Rxra-null, Rxra^af1o, Rxra^af2o, and Rara-, Rarb-, Rarg-null mutants are observed in compound Rxra/Rara-, Rxra/Rarb-, and Rxra/Rarg-null mutants (Xα/Aα, Xα/Aβ and Xα/Aγ), in compound Rxra^af2o/Rara-, Rxra^af2o/Rarb-, and Rxra^af2o/Rarg-null mutants (Xαaf2o/Aα, Xαaf2o/Aβ and Xαaf2o/Aγ), in compound Rxra^af1o/Rara-, Rxra^af1o/Rarb-, and Rxra^af1o/Rarg-null mutants (Xαaf1o/Aα, Xαaf1o/Aβ and Xαaf1o/Aγ), as well as in compound Rara/b-, Rara/g- and Rarb/g-null mutants (Aα/Aβ, Aα/Aγ and Aβ/Aγ). *: this abnormality is present in a majority of the mutants. #: this abnormality is fully penetrant. VAD, these abnormalities belong to the fetal vitamin A deficiency syndrome (Wilson et al., 1953). From references (Kastner et al., 1997a and 1997b; Mascrez et al., 1998; Kastner et al., 1994; Mascrez et al., 2001).