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Fig. 6. isl and Lim3 genetically interact with beat Ic in TN axon targeting and fasciculation. (A) In situ hybridization of beat Ic in a wild-type stage 15 VNC. Expression is evident in lateral clusters (arrows) but not in the RP neurons (arrowhead). (B) In situ hybridization and antibody labeling in a Lim3B-Gal4;UAS-taumycEGFP late stage 15 embryo. Both GFP (brown) and beat Ic (blue) expression is observed in the TN neurons (arrow). The cluster of RP neurons (arrowhead) stain very darkly for GFP expression but do not express beat Ic (see A). (C) Embryos that lack beat Ic were generated using the overlapping chromosomal deficiencies, beat Ic^Df/beat Ic^Df1(Df(2L)TE35D-GW19/Df(2L)RM5). In these embryos, the TMNp motor axon did not completely fasciculate with the LBD projection, resulting in bifurcation (arrow) and aberrant ventral muscle exploration. (D) In isl mutants, isl^37Aa/isl^Df embryos, the same failure of the TMNp motor axon to fasciculate with the LBD projection is observed (arrow). (E,F) TN targeting and fasciculation is also affected (arrows) in embryos in which one copy of isl, Lim3 and beat Ic have been removed, isl^37Aa Lim3^BD6 beat Ic^Df (C) and isl^37Aa Lim3^BD6/beat Ic^Df1 (E). (G) Schematic diagram of the beat Ic locus. Isl1 (CTAATG) and Lhx3 (AATTAATTA) consensus sites within this locus are graphically represented.

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