Egfr -dependent expression of genes in the embryo. In zygotic null Egfr mutants both otd and FasIII expression are lost. In ebi mutant embryos lacking both maternal and zygotic contribution, FasIII expression is largely abolished, although some residual patches of staining remain. In ebi mutant embryos, otd expression is markedly reduced. These data suggest that ebi may be a component in the Egfr signal transduction pathway.
Torso controls the development of the anterior and posterior termini of the embryo.
Ras, Raf, MEK, and MAPK participate in both the Egfr and Torso RTK pathways. In summary, ebi mutant phenotypes assessed using both molecular and morphological criteria are similar to Egfr mutations. Furthermore, ebi does not function in all RTK pathways, since Torso-induced terminal development is ebi independent. These data indicate that ebi , either directly or indirectly, regulates Egfr signaling. The R7 equivalence group comprises five cells competent to become R7 neurons.