There is an unhealthy tendency in our media-saturated society to value only those things that receive the most hype. Our interests and opinions about the popular world are shaped by the tabloids that we all secretly read in supermarket checkout lines,which only enlighten us about Oscar winners, Most Valuable Players, supermodels, and the super rich. Our senses are seldom assaulted with stories about the less-visible members of the supporting cast. We rarely read about the legions of extraordinarilytalented people who croon back-up vocals or who constitute an unassailable offensive line. I submit that we scientists are not infrequently guilty of this sort of cultish behavior when we stratify the relative importance of biological systems and their associated unanswered questions. When I think about the eye, for example, I tend to think about the marquee players. I envision rods and cones, replete with rhodopsin, transducin, and cGMP-gated channels. I confess that I don't tend to occupy my mind withthe multitude of other cell types and pathways that must be in place for the photosensitive cell types to work their magic. The Emerging Topic in this issue by Hartzell et al. makes it abundantly clear just how myopic a viewpoint this is. Photoreceptorcells are constantly being trimmed by the phagocytic cells of the retinal pigment epithelium. The pigment that these cells ingest needs to be degraded. If its destruction is impeded it can accumulate in the retinal pigment epithelium, compromising thesecells' functional capacity, potentially leading to retinal damage. Mutations in the genes encoding the bestrophin chloride channels are responsible for Best's macular dystrophy, a heritable form of macular degeneration.
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