Abstract
The Retinal homeobox gene (Rx; also Rax) plays a crucial role in the early development of the vertebrate eye. Germline deletion of Rx in mice results in the failure of optic vesicle formation, leading to anophthalmia. Recent research using conditional mouse knockout models provides some clues to the role of Rx in eye development following optic vesicle formation. However, the functions of Rx in embryonic retinogenesis are still not fully understood. We investigated the function of Rx in the mouse neural retina using a conditional knockout where the Pax6α-Cre driver deletes Rx activity in early retinal progenitors. The deletion of Rx activity causes a loss of retinal lamination, a depletion of retinal progenitors, and a change in retinal cell fate in our conditional knockout model. The deletion of Rx leads to an absence of late-born retinal neurons (rods and bipolar cells) and Müller glia at postnatal ages, as well as a loss of the early-born cone photoreceptors. Decreased BrdU labeling in the Rx-deleted portion of the retina suggests a loss of retinal progenitors via early cell cycle exit, which likely prevents the formation of late-born cells. As early-born cells, cone photoreceptors should not be as affected by early cell cycle exit of retinal progenitors. However, embryonic cone photoreceptor labeling is also markedly reduced in Rx-deleted retinas. Together these data demonstrate the importance of Rx for retinal progenitor proliferation and a specific requirement of Rx for cone formation in mice.