RA is required for proper patterning and neurogenesis within the spinal cord ([Diez del Corral and Storey, 2004; Maden, 2006; Wilson and Maden, 2005] and references therein), and conditional gene knockouts have shown that it acts in a complex manner, being produced both by the adjacent mesoderm, and eventually, by specific motor neuron progenitor populations at brachial and lumbar levels [Ji et al., 2006; Vermot et al., 2005b]. RARα and RARβ may act redundantly to transduce the RA signal within the spinal cord, as the corresponding null mutant mice do not display phenotypic abnormalities that may be related to abnormal spinal cord development. Molecular patterning of the spinal cord has yet to be studied in compound Rara/Rarb mutants.
