Dachshund and eyes absent proteins form a complex and function synergistically to induce ectopic eye development in Drosophila.
The eyeless, dachshund, and eyes absent genes encode conserved, nuclear proteins that are essential for eye development in Drosophila. Misexpression of eyeless or dachshund is also sufficient to induce the formation of ectopic compound eyes. Here we show that the dachshund and eyes absent genes act synergistically to induce ectopic retinal development and positively regulate the expression of each other. Moreover, we show that the Dachshund and Eyes Absent proteins can physically interact through conserved domains, suggesting a molecular basis for the genetic synergy observed and that a similar complex may function in mammals. We propose that a conserved regulatory network, rather than a linear hierarchy, controls retinal specification and involves multiple protein complexes that function during distinct steps of eye development.
Chen
R
R
Department of Pathology, Baylor College of Medicine, Houston, Texas 77030, USA.
Amoui
M
M
Zhang
Z
Z
Mardon
G
G
D000818:Animals; D002454:Cell Differentiation; D004330:Drosophila; D029721:Drosophila Proteins; D004357:Drug Synergism; D005136:Eye Proteins / Q000235:genetics / Q000502:physiology*; D019476:Insect Proteins / Q000235:genetics / Q000502:physiology*; D009687:Nuclear Proteins / Q000235:genetics / Q000502:physiology*; D017956:Photoreceptor Cells, Invertebrate / Q000196:embryology*; D011485:Protein Binding; D012160:Retina / Q000196:embryology / Q000254:growth & development; D014158:Transcription, Genetic
D029721:Drosophila Proteins; D005136:Eye Proteins; D019476:Insect Proteins; D009687:Nuclear Proteins; C103968:dac protein, Drosophila; C092694:eya protein, Drosophila