CREST, JRDC and Dept. of Molecular Neurobiology, Inst. of Basic Med. Sci. and Center for TARA, Univ. of Tsukuba, Japan FAX: 81-298-53-6966 e-meil:okabe@md.tsukuba.ac.jp
The development of embryonic chordotonal (Ch) organs in the PNS begins at the germband extended stage with a cluster of cells in the dorsal ectoderm expressing the atonal (ato) gene that is a proneural gene for both Ch organs and photoreceptor cells. Only five Ch organ precursors (COPs) express ato mRNA in the middle of embryogenesis, although eight Ch organs (five in LCh5, V'Ch1, VChA and VChB) are usually observed in each abdominal hemisegment. The cell-lineage explaining how these five ato-expressing COPs ultimately supply eight Ch organs remains to be unsolved. The rhomboid (rho) gene, which encodes an integral membrane protein, probably plays a role in the process of generating three of eight Ch organs, because the rho loss of function mutant has only five Ch organs in each abdominal hemisegment due to loss of VChB and two Ch organs in LCh5. The rho transcripts expressed in five ato-expressing COPs and this rho expression was absent in the ato null mutant. These results indicated that rho expressions in five ato-expressing COPs were necessary to form the three Ch organs that were absent in the rho loss of function mutant. On the other hand, we previously showed that argos, which encodes a diffusible inhibitor of Drosophila EGF receptor (DER) /Ras1 signaling, negatively regulated the number of Ch organs (COPs). Together with the phenotype of rho that can promote DER/Ras1 signaling, these results support the possibility that DER/Ras1 signaling is essential for the generation of three of eight Ch organs (VChB and two in LCh5). To confirm this possibility, we examined Ch organ phenotypes of mutants of DER/Ras1 signaling components. The elimination of DER/Ras1 signaling resulted in a loss of three of eight Ch organs (VChB and two in LCh5), while the hyperactivation of DER/Ras1 signaling caused the formation of additional Ch organs. The development of remaining five Ch organs (V'Ch1, VChA and five in LCh5) was unaffected in these DER/Ras1 signaling mutants and the rho mutant. These results indicate that DER/Ras1 signaling and rho are necessary to form three of eight Ch organs (VChB and two in LCh5). We also examine the argos expression in cells surrounding COPs in genetic backgrounds of mutants eliminating DER/Ras1 signaling pathway and rho. argos transcripts were completely absent or greatly reduced in these mutants. These results indicated that argos seems to mediate the inhibitory feedback loop of DER/Ras1 signaling to prevent generating additional Ch organs by limiting the DER/Ras1 signaling activity. The cell lineage of eight COPs and the analogy between Ch organ and photoreceptor developments will be discussed.