Vision begins in the outer segments of rod (which perceive dim light, only in black and white) and cone (bright light and color) photoreceptor cells of the retina. In these cells, visual pigment molecules absorb photons, become activated and initiate the phototransduction, or visual, cascade (Figure 1). One aspect of this research program strives to identify the genes implicated in the cause of retinal degenerations in human and animal models. Of the estimated three to four dozen genes thought to be involved in phototransduction and its regulation in mammalian rod photoreceptors, about half have been cloned.  To character-ize gene products and to follow the consequence of a specific mutation, we express genes or cDNAs either in vitro by using unicellular systems (such as insect cells) infected with baculovirus constructs, or in vivo by using transgenic/knockout mice. To date, genes encoding rhodopsin, the transducin a subunit, the catalytic PDE subunits, the CNG channel subunits, and the GC1/GCAP1 modulatory unit have been shown to carry point mutations and/or microdeletions that cause retinal degeneration (autosomal dominant or recessive dystrophies). Several naturally occurring animal models for retinal degeneration (Figure 1) are of particular interest to us in determining the mechanism of cell death.