Novel dominant-negative mutation within the six domain of the conserved eye specification gene sine oculis inhibits eye development in Drosophila.

Abstract

The development of the compound eye of Drosophila is controlled, in part, by the concerted actions of several nuclear proteins that form an intricate regulatory system. One member of this network is sine oculis (so), the founding member of the Six gene family. Mutations within so affect the entire visual system, including the compound eye. The vertebrate homologs Six3 and Six6 also appear to play crucial roles in retinal formation. Mutations in Six3 inhibit retinal formation in chickens and fish, whereas those in Six6 are the underlying cause of bilateral anophthalmia in humans. Together, these phenotypes suggest a conserved role for the Six genes in eye development. In this report, we describe the effects of a dominant-negative mutation of sine oculis on the development of the compound eye of Drosophila. The mutation resides within the Six domain and may have implications for eye development and disease.

• Authors: Kristin Roederer, Loralyn Cozy, Jason Anderson, Justin P Kumar
• Journal: Developmental dynamics : an official publication of the American Association of Anatomists (Dev Dyn) Vol. 232 Issue 3 Pg. 753-66 (Mar 2005) ISSN: 1058-8388 [Print] United States
• PMID: 15704100 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, U.S. Gov't, P.H.S.)
• Copyright: Copyright (c) 2005 Wiley-Liss, Inc.

Chemical References

• Drosophila Proteins
• Eye Proteins
• Homeodomain Proteins
• So protein, Drosophila

Topics

• Animals
• Drosophila (embryology, genetics, ultrastructure)
• Drosophila Proteins (chemistry, genetics, metabolism, ultrastructure)
• Embryo, Nonmammalian (ultrastructure)
• Eye (embryology, metabolism, ultrastructure)
• Eye Proteins (chemistry, genetics, metabolism, ultrastructure)
• Gene Expression Regulation, Developmental
• Genes, Dominant
• Genes, Homeobox
• Homeodomain Proteins (chemistry, genetics, metabolism, ultrastructure)
• Models, Anatomic
• Mutation
• Protein Structure, Tertiary