The Drosophila eye consists of a reiterative hexagonal array of photor
eceptor cell clusters, the ommatidia. During normal morphogenesis, the
clusters in the dorsal or ventral halves of the disc rotate 90 degree
s in opposite directions, forming mirror images across a dorsoventral
equator. In the mutant nemo (nmo), there is an initial turning of appr
oximately 45 degrees, but further rotation is blocked. Genetic mosaic
analysis indicates that the nmo gene acts upon each cluster as a whole
; normal nmo function in one or more photoreceptor cells appears to be
sufficient to induce full rotation. The nmo gene sequence encodes a s
erine/threonine protein kinase homolog, suggesting that the kinase is
required to initiate the second step of rotation. In another mutant, r
oulette, excessive rotation through varying angles occurs in many omma
tidia. This defect is suppressed by nmo, indicating that nmo acts upst
ream in a rotation-regulating pathway.