Fig. 4. Opposing genetic roles of shn and brk in formation of PNS neurons. (A-D) Flat preparations of stage 16 embryos showing one thoracic (T3) and four abdominal (A1-A4) segments with PNS neurons visualized with the 22C10 antibody. Regions that harbor neurons that belong to the dorsal, lateral or ventral clusters are color-coded blue, yellow and red, respectively. (A) brk^m68 homozygous embryo with normal numbers of abdominal PNS neurons in dorsal and lateral clusters, but fewer in ventral clusters (compare with Fig. 2D). (B) Homozygous shn¹ embryos display a dramatic reduction in neuronal numbers and disorganization in the dorsal and lateral clusters, but less so in ventral clusters (compare with Fig. 2B). The compact appearance of the PNS is due to a lack of dorsal closure (dorsal extension of the epidermis) in these animals. Double homozygous embryos for brk^m68;shn^k04412 (C) and brk^m68;shn¹ (D) display a clear rescue in neuronal numbers relative to the single shn mutant (A); this rescue can be observed in dorsal and lateral but not in ventral clusters. The correct positioning of the pentascolopodial organ and dorsal closure are also restored in these double mutants (brackets; compare with Fig. 2E,H). (E) Mean values and standard error of the number of neurons in the dorsal, lateral and ventral clusters in abdominal segments with different genetic backgrounds. shn and brk have opposite roles in the dorsal and lateral clusters as brk;shn double mutants have more neurons than shn mutants alone. In the ventral cluster, brk appears to act independently of shn as brk;shn double mutants have comparable numbers of neurons to brk single mutants. WT, n=63; shn^k04412, n=116; brk^m68, n=121; brk^m68;shn^k04412, n=74; shn¹, n=37; brk^m68;shn¹, n=27.

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