Fig. 3. Spatially localized JAK/STAT signaling is required for hindgut elongation and cell rearrangement. Compared with wild type (A), the hindgut is shorter and wider in upd^os1A (B), hop^m-z- (C) and Stat92E^m-z- (D) embryos. As seen in transverse section, compared with wild-type (E), there are more cells in the hindgut circumference of upd^os1A (F), hop^m-z- (G) and Stat92E^m-z- (H) embryos. The hindgut is also shorter and wider when bynGAL4 is used to drive uniform hindgut expression of UAS constructs that activate JAK/STAT signaling, namely UAS-upd (J) and UAS-hop^TML (K); the defect is more severe when both UAS-hop^TML and UAS-Stat92E are driven together (L). Inhibition of JAK/STAT signaling by bynGAL4 driven expression of the dominant negative UAS-dome^CYT3.2 also results in a shorter, wider hindgut (I); transverse sections of embryos of these genotypes similarly reveal a greater than normal number of cells in the hindgut circumference (M-P). All embryos shown are at stage 16; wholemounts are stained with anti-Crb and sections are of the large intestine. Averages of total number of hindgut cells, cells in hindgut circumference, and hindgut lengths observed in the loss-of-function mutants and in bynGAL4 embryos expressing various JAK/STAT components are summarized in(Q.

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