Fig. 1.

Yorkie induces ISC/Eb overproliferation in the gut epithelium. (A) The ISC lineage. (B) Esg(+) ISC/Eb cells in the wild-type posterior midgut epithelium stained with anti-Yki antibody. (C) Shown are: (i) wild type (w¹¹¹⁸/+; MST1096-Gal4/+) versus (ii) Yorkie RNAi (MST1096-Gal4/+; yki RNAi-1/+) adult wings. (D) Confocal micrographs of wild type (first panel is esg>GFP: w¹¹¹⁸/+; esg-Gal4, UAS-GFP, Tub-Gal80^TS/+), RNAi against yki (middle panel is esg>yki RNAi-1: esg-Gal4, UAS-GFP, Tub-Gal80^TS/+; yki RNAi-1/+) and overexpression of yki (left panel is esg>yki: esg-Gal4, UAS-GFP, Tub-Gal80^TS/+; UAS-yki/+). The same hairpin that reduces wing size in C has no effect on ISC proliferation, whereas yki overexpression causes overproliferation. (E) Quantification of total mitoses in the entire midgut (left), and the frequency of Esg(+) cells in one field of view (FOV) in the posterior region of the midgut (right). All constructs were expressed in ISC/Eb cells. Both Yki and mutated Yki (Yki^S168A) accelerated cell division, whereas RNAi constructs against yki produced no apparent changes when compared with wild type (Ctrl). Error bars indicate s.e.m. (P<0.05). (F) Confocal images showing Yki-overexpressing clones (shown on right, yki is hsFlp/+; UAS-GFP, act>CD2>Gal4/+; UAS-yki/+) and wild-type clones (left, w¹¹¹⁸ is hsFlp/+; UAS-GFP, act>CD2>Gal4/+). Clones mutant for yki (yki^B5 is hsFlp, Tub-Gal4, UAS-nlsGFP/+; FRT42D, Tub-Gal80^TS/FRT42D yki^B5) are no different from wild-type (arm-LacZ is hsFlp, Tub-Gal4, UAS-nlsGFP/+; FRT42D, Tub-Gal80^TS/FRT42D arm-LacZ).