Induction of Ectopic Eyes by Targeted Expression of the <i>eyeless</i> Gene in <i>Drosophila</i>

TLDR

The Drosophila eyeless gene encodes a transcription factor homologous to Pax‑6, and loss‑of‑function mutations cause eye defects, indicating its essential role in eye morphogenesis. Targeted expression of ey cDNA in various imaginal disc primordia induced ectopic eye structures on wings, legs, and antennae. The induced ectopic eyes were morphologically normal with fully differentiated ommatidia and photoreceptors, supporting ey as a master control gene for eye morphogenesis across metazoa.

Abstract

The Drosophila gene eyeless ( ey ) encodes a transcription factor with both a paired domain and a homeodomain. It is homologous to the mouse Small eye ( Pax-6 ) gene and to the Aniridia gene in humans. These genes share extensive sequence identity, the position of three intron splice sites is conserved, and these genes are expressed similarly in the developing nervous system and in the eye during morphogenesis. Loss-of-function mutations in both the insect and in the mammalian genes have been shown to lead to a reduction or absence of eye structures, which suggests that ey functions in eye morphogenesis. By targeted expression of the ey complementary DNA in various imaginal disc primordia of Drosophila , ectopic eye structures were induced on the wings, the legs, and on the antennae. The ectopic eyes appeared morphologically normal and consisted of groups of fully differentiated ommatidia with a complete set of photoreceptor cells. These results support the proposition that ey is the master control gene for eye morphogenesis. Because homologous genes are present in vertebrates, ascidians, insects, cephalopods, and nemerteans, ey may function as a master control gene throughout the metazoa.