Laboratory of Applied Entomology, School of Agriculture, University of Tokyo, ~ Department of Biology, University of Kyusyu, § Mitsubishi-Kasei Institute of Life Sciences, Tokyo, Japan,
The canoe (cno) gene encodes a protein necessary for normal development of a variety of imaginal structures including the compound eyes, bristles and wings as well as of embryos. The cno gene product contains three distinct sequence motifs, the U104 kinesin-like domain, class V myosin-like domain, and the DHR/PDZ domain. Since CNO has been shown to bind to GTP-Ha-RAS in vitro, we examined its in vivo function in RAS signaling in the developing eye. The sev-Ras1[Val12] transgene expression results in over production of cone cells in the compound eye, and this phenotype is dominantly enhanced by cno[10B1], a loss-of-function allele of canoe. The raf[c110] mutation completely suppresses the effects of sev-Ras1[Val12] and cno[10B1], indicating that raf is epistatic to Ras1 and cno. The excess cone cells seem to differentiate from precursors which would otherwise undergo programmed cell death. We hypothesize that CNO forms an inactive complex with RAS1 in undifferentiated retinal precursor cells, thereby preventing them from developing into cone cells.