Fig. 4. SoxNeuro; Dichaete double mutant embryos are far more severely affected than either single mutant. Whole-mount ventral views of stage 16 (A-D), stage 8 (E) and stage 9 (F) SoxNeuro^U6–35; D^r72 double mutant embryos stained with BP102 (A,B), anti-Eve (C,D), anti-Achaete (E,F) and anti-Hb (H,I). (A,B) Double mutant embryos show a variable severe hypoplasia; longitudinal axons are almost totally absent and there are frequent gaps in the neuropil. (C,D) As in SoxNeuro^U6–35, RP2 and ELC staining is variably absent in double mutant embryos; in addition, we see a loss of aCC/pCC and CQ cells in 15% of hemisegments (arrowheads). The defects in D are much more extreme than can be accounted for by the Dichaete segmentation phenotype, suggesting that many segments fail to express Eve in any cells. (E,F) Achaete protein is absent laterally in SoxNeuro; Dichaete embryos as in SoxNeuro^U6–35; however, Achaete is now undetectable in 54% of medial clusters (arrowheads); Achaete staining is completely absent in 21% of segments (arrowheads). (G) Diagrammatic representation of S1 neuroblasts at late stage 8. Neuroblasts are arranged in an orthogonal array of four rows and three columns [medial (M), intermediate (I) and lateral (L)]. (H,I) Late stage 8 D72 (H) and SoxN^U6–35; D^r72 (I) embryos. S1 neuroblasts are barely affected in Dichaete mutant embryos [e.g. NB5-3 (arrowhead) is missing in 2% of hemisegments]. As in SoxN^U6–35, lateral NBs are frequently absent in double mutant embryos; in addition, within the intermediate column we observe Hb-expressing cells in only 21% of hemisegments compared with 48% in SoxN mutants (arrowheads). In I, we are unable to unambiguously identify these cells as NB 5-3.

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