Fig. 2.

Genetic interactions between fishand dfr in CNS midline gene expression and development. Anti-β-gal immunostaining of stage 15 wild-type (A), fish⁸⁷(B), dfr^E82(C), anddfr^E82-fish⁸⁷double mutant (D) embryos carrying the P[1.0slit-lacZ] marker. In addition, anti-β-gal immunostaining was also performed on stage 15 wild-type (E) anddfr^E82-fish⁸⁷double mutant (F) embryos carrying the P[3.7sim-lacZ] marker. A, Note the predominantly dorsal positions of P[1.0slit-lacZ]-expressing midline glia in each segment of the ventral nerve cord in a wild-type embryo.B, In fish⁸⁷ mutant embryos there is a loss and disorganization of P[1.0slit-lacZ]-expressing midline cells.C, In dfr^E82 mutant embryos there is only modest misplacement of P[1.0slit-lacZ]-expressing midline cells.D, Indfr^E82-fish⁸⁷double mutant embryos there is a dramatic loss of P[1.0slit-lacZ]-expressing cells. This phenotype is much more severe than that seen in eitherfish⁸⁷ (B) ordfr^E82 (C) single mutant embryos. E, In wild-type embryos the CNS midline cells express sim and are organized into segmentally reiterated clusters of cells along the ventral nerve cord.F, Indfr^E82-fish⁸⁷double mutant embryos there is a severe decrease in simexpression and disorganization of midline cells. All views are sagittal with anterior to left.