Fig. 4. Analysis of ASEL and ASER fate in fozi-1 and lim-6 mutant animals. (A) In fozi-1(cc607)-null mutant animals, ASEL-specific lim-6^prom::gfp (otIs114), flp-4^prom::gfp (otIs178), gcy-7 ^prom::gfp (otIs3) and gcy-6 ^prom::gfp (otIs162) are de-repressed in ASER. `0=0' indicates no expression, `L>0' indicates exclusive expression in ASEL, `L>R' indicates expression in ASEL is stronger than in ASER, `L=R' indicates equal expression in ASEL and ASER, `L<R' indicates expression in ASER is stronger than in ASEL, and `0<R' indicates exclusive expression in ASER. (B) Analysis of ASER fate markers in fozi-1(cc607) null mutants. Reporter arrays used were ntIs1 (gcy-5), otEx2409 (gcy-4) and otEx1274 (hen-1^ASER). (C) Summary of the fozi-1 mutant phenotype and comparison with previously described ASE fate mutants. Blue circles indicate the ASEL-specific gene expression battery, red circles indicate the ASER-specific gene expression battery. (D) lim-6 is not sufficient to repress ASER cell fate. (E) Summary of genetic interaction data. The incomplete expressivity of fozi-1 and lim-6 null alleles argues for the existence of parallel pathways (indicated by factor X, Y, Z). The two different scenarios make different predictions about the site of action of the parallel pathways. In scenario 1, it is active in ASER; in scenario 2, it is active in ASEL.