Removal of clock gene <i>Bmal1</i> from the retina affects retinal development and accelerates cone photoreceptor degeneration during aging

Abstract

Significance Circadian rhythms are not simply a passive consequence of cyclic fluctuations in the environment, but instead originate within the organism. Accumulating evidence indicates that disruption of circadian rhythms contributes to the development of many diseases. Here, we demonstrate that removal of the clock gene Bmal1 from the retina has multiple effects on rod and cone pathways. In the cone pathway, the primary effect is on cone viability, an effect accentuated in aging mice. In the rod pathway, we observed that retinal Bmal1 removal caused stunting of rod bipolar cell dendrites and thinning of the outer plexiform layer in both young and old mice. Hence, our data suggest that circadian clock dysfunction contributes to aberrant visual function during development and aging.