The sevenless (sev) cascade plays an inductive role in formation of the R7 photoreceptor, whilst the pokkuri (pok) and tramtrack (ttk) gene products are known to repress R7 induction in developing ommatidia of Drosophila melanogaster. To elucidate how these positive and negative signalling mechanisms co-operate in the normal fate determination of R7, genetic interactions of mutations in the pok locus with ttk and downstream elements of sev including Gap1, raf1, rolled (rl) and seven in absentia (sina) were examined. The eye phenotype of a weak hypomorph, pok15, was enhanced dominantly by Gap1(mip), a recessive mutation in a gene encoding a down-regulator of Ras1, producing multiple R7 in ommatidia. Ras1 has been reported to activate rl-encoded mitrogen-activated protein (MAP) kinase via Raf1 that is associated physically with Ras1. Ommatidia of raf1(c110) and rl2/rl(EMS64) typically lacked R7 and a few outer- photoreceptors. The pok1 mutation suppressed dominantly the raf1(c110) and rl2/rl(EMS64) eye phenotypes, allowing single R7 cells to develop in ommatidia. The raf1(c110) mutation improved adult viability of pok1 homozygotes. An in vitro experiment demonstrated that MAP kinase phosphorylates Pok protein. Ttk is a transcriptional repressor which binds to the regulatory sequence upstream of the fushi-tarazu (ftz), even skipped (eve) and engrailed (en) coding region. A reduced activity in ttk resulted in enhancement of the pok phenotype, ttk mutations produced extra R7 cells even in sina homozygotes whilst the pok mutation did not. This result indicates that Ttk represses R7 induction downstream of the sites where Pok and Sina function.
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