During Drosophila ommatidial development, a single cell is selected wi
thin the ommatidial cluster to become the R7 photoreceptor neuron. The
seven-up gene has been shown to play a role in this process by preven
ting four other photoreceptor precursors, R3/R4/R1/R6, from adopting t
he R7 cell fate. The seven-up gene encodes a steroid receptor-like mol
ecule that is expressed only in those four cells that require seven-up
function in the developing Drosophila ommatidium. We have examined th
e functional significance of the spatially restricted expression of se
ven-up by misexpressing seven-up isoforms. As expected from the functi
on that seven-up performs in R3/R4/R1/R6, ubiquitous expression of sev
en-up causes transformation of the R7 cell to an R1-R6 cell fate. In a
ddition. depending on the timing and spatial pattern of expression, va
rious other phenotypes are produced including the loss of the R7 cell
and the formation of extra R7 cells. Ubiquitous expression of seven-up
close to the morphogenetic furrow interferes with R8 differentiation
resulting in failure to express the boss protein, the ligand for the s
evenless receptor tyrosine kinase, and the R7 cell is lost consequentl
y. Extra R7 cells are formed by recruiting non-neuronal cone cells as
photoreceptor neurons in a sevenless and bride of sevenless independen
t way. Thus, the spatiotemporal pattern of seven-up expression plays a
n essential role in controlling the number and cellular origin of the
R7 neuron in the ommatidium. Our results also suggest that seven-up co
ntrols decisions not only between photoreceptor subtypes, but also bet
ween neuronal and non-neuronal fates.