Fig. 4
Bursicon acts on rk-expressing neurons to cause melanization and sclerotization. a Abdominal pigmentation in 3-h- (upper panel) and 48-h-old (lower panel) female flies expressing tBur or rk RNAi transgenes under the control of pan-neuronal drivers (elav-GAL4 and nsyb-GAL4). b Abdominal pigmentation in 3-h- (upper panel) and 48-h-old (lower panel) female flies expressing tBur or rk RNAi transgenes under the control of rk-GAL4 and restricted to non-neuronal rk cells using elav-Gal80. c Rescue of abdominal pigmentation in 3-h- (upper panel) and 48-h-old (lower panel) female rk1/rk4 flies expressing a rk cDNA [19] under the control of the rk-GAL4, TH-GAL4, and elav-GAL4, drivers. In a–c, boxes indicate the first and third quartiles, thick central lines mark the medians, and whiskers represent data range. Red dashed lines indicate the median pigmentation level when tBur is expressed ubiquitously (rk>tBur). Results for each age were compared using a one-way ANOVA followed by Tukey HSD post hoc analysis. Different letters indicate statistically significant differences (p values < 0.01); NS: not significantly different. n = 10 for each group. d Quantification of soluble cuticular proteins extracted from wings and abdominal epidermis of elav>tBur, rk>tBur female flies with or without elav-GAL80, in three separate experiments; median is indicated by short horizontal line. For quantification of other proteins (indicated in Additional file 1: Figure S2B) see Additional file 1: Figure S7. Different letters indicate statistically significant differences (one-way ANOVA followed by Tukey HSD, p < 0.02). Genotypes are coded as described in Fig. 1b