In Drosophila, rhodopsin (ninaE) is expressed in photoreceptors R1–R6. In ninaE null mutants, the rhabdomere, a structure analogous to vertebrate outer segments, fails to develop in R1–R6 photoreceptors [42], reminiscent of the situation in rhodopsin-/- mice [29]. An intriguing experiment by Kumar et al. [43] demonstrated a temporal requirement for rhodopsin expression during rhabdomere development. In ninaE null flies, a ninaE transgene under the control of a heat shock promoter was subjected to various temperature shifts during development. Heat shock during the normal time of rhodopsin onset resulted in substantial and long-lasting rescue of photoreceptor structure and transient rescue of photoreceptor physiology. However, expression shortly before or after this critical period failed to rescue, suggesting that rhodopsin expression during a discrete window of time in development is essential for proper rhabdomere morphogenesis. This result is consistent with observations in the rat wherein rhodopsin onset occurs with strict timing in the developmental history of most rods in vivo [44]. Thus, through its regulation of rhodopsin levels, or perhaps through control of the kinetics of the up-regulation of rhodopsin beginning at about P6, Crx may be regulating outer segment morphogenesis. The similarty of the two cases may extend further. At present, the closest Crx relative in Drosophila is Otd, the founding member of the class of homeobox genes to which Crx belongs. Interestingly, in one hypomorphic allele of Drosophila otd, otduvi, photoreceptor morphogenesis is also disrupted [45].