Signaling by the TGF-beta homolog decapentaplegic functions reiteratively within the network of genes controlling retinal cell fate determination in Drosophila.

Departments of Pathology, Molecular and Human Genetics and Ophthalmology, and Program in Developmental Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Retinal cell fate determination in Drosophila is controlled by an interactive network of genes, including eyeless, eyes absent, sine oculis and dachshund. We have investigated the role of the TGF-beta homolog decapentaplegic in this pathway. We demonstrate that, during eye development, while eyeless transcription does not depend on decapentaplegic activity, the expression of eyes absent, sine oculis and dachshund are greatly reduced in a decapentaplegic mutant background. We also show that decapentaplegic signaling acts synergistically with and at multiple levels of the retinal determination network to induce eyes absent, sine oculis and dachshund expression and ectopic eye formation. These results suggest a mechanism by which a general patterning signal such as Decapentaplegic cooperates reiteratively with tissue-specific factors to determine distinct cell fates during development.
Mesh Terms:
Animals, Cell Differentiation, DNA-Binding Proteins, Drosophila, Drosophila Proteins, Eye Proteins, Gene Expression Regulation, Developmental, Insect Proteins, Nuclear Proteins, Retina, Signal Transduction, Transforming Growth Factor beta
Development Feb. 01, 1999; 126(5);935-43 [PUBMED:9927595]
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