ion pathways [8,10]. Crx transcripts begin to be expressed in developing photoreceptors at embryonic day 12.5 (E12.5) in the mouse and a strong upregulation of Crx transcription is apparent across the differentiating photoreceptors at postnatal day 6 (P6). Photoreceptor cells in the Crx knockout (KO) mice exhibit a dramatic reduction of many photoreceptor molecules including visual pigments and develop neither photoreceptor outer segments nor a synaptic terminus [8,10]. In addition, mutations of human CRX have been demonstrated to be associated with three types of photoreceptor diseases: autosomal dominant cone-rod dystrophy 2, autosomal dominant-type retinitis pigmentosa, and Leber's congenital amaurosis (LCA) [11-14]. While Otx2 and Crx control general photoreceptor development, three other transcription factors, TRβ2, Nrl, and Nr2e3 regulate the specification of photoreceptor cell types [4,5,7].
SAM domains (a