Laboratory beagle dogs with an apparent absence of atapetum lucidumwere identified by ophthalmoscopic examination. Breeding experiments demonstrated a probable autosomal recessive mutation. Studies of the development of the tapetal abnormality showed that up to postnatal day 21 the tapetum was normal by light and ultrastructural morphology. Subsequent to that time the tapetal rodlets failed to accumulate electron-dense material, did not accumulate zinc, and degenerated primarily into spherical inclusion bodies of varying electron density. In the early phases of the degeneration the rough endoplasmic reticulum formed large whorls of membrane denuded of ribosomes. With time, the inclusions became electron lucent, and the entire tapetal cell degenerated, ending with almost total loss of thetapetum lucidumby approximately one to two years of age. The structure of the retina was normal. Retinal function measured by electroretinography was normal except for a slight elevation of dark adapted white light thresholds. It is speculated that the hereditary defect may be defective synthesis of the tapetal rodlet matrix or of the zinc-complexing substance of the tapetum.