CELL FATE CONTROL IN THE DROSOPHILA RETINA BY THE ORPHAN RECEPTOR 7-UP - ITS ROLE IN THE DECISIONS MEDIATED BY THE RAS SIGNALING PATHWAY

Citation
S. Kramer et al., CELL FATE CONTROL IN THE DROSOPHILA RETINA BY THE ORPHAN RECEPTOR 7-UP - ITS ROLE IN THE DECISIONS MEDIATED BY THE RAS SIGNALING PATHWAY, Development, 121(5), 1995, pp. 1361-1372
Citations number
65
Categorie Soggetti
Developmental Biology
Journal title
ISSN journal
09501991
Volume
121
Issue
5
Year of publication
1995
Pages
1361 - 1372
Database
ISI
SICI code
0950-1991(1995)121:5<1361:CFCITD>2.0.ZU;2-V
Abstract
Drosophila seven-up is an orphan receptor of the steroid receptor fami ly that is required to specify photoreceptor neuron subtypes in the de veloping compound eye. Expression of seven-up is confined to four of t he eight photoreceptor precursors, R3/R4/R1/R6. We show that misexpres sion of seven-up in any of the other cell types within the developing ommatidium interferes with their differentiation. Each cell type respo nds differently to seven-up misexpression, For example, ectopic expres sion in the non-neuronal cone cells using the sevenless promoter/enhan cer (sev-svp) causes the cone cells to take on a neuronal identity. Ec topic expression of seven-up in R2/R5 using the rough enhancer (ro-svp ) causes these neurons to lose aspects of their photoreceptor subtype identity while remaining neuronal. Each cell type appears to have a di fferent developmental time window that is sensitive to misexpressed se ven-up. The temporal order of responsiveness of each cell type to mise xpressed seven-up is similar but not identical to the order of neurona l differentiation. This suggests that there are processes of specifica tion that are distinct from the specification to become a photorecepto r neuron. We have identified members of the ras signaling pathway as s uppressors of the cone cell to R7 neuron transformation caused by sev- svp. Suppression of the sev-svp phenotype can be achieved by decreasin g the gene-dosage of any of the members of the ras-pathway. This sugge sts that the function of seven-up in the cone cells requires ras signa ling. However, a decrease in ras signaling results in enhancement of t he phenotype caused by the ro-svp transgene. We discuss the relationsh ip between decisions controlled by seven-up and those controlled by ra s signaling.