Fig. 4.

Yki accelerates ISC division during regeneration. (A) The Yki-depleted midgut (bottom panel is esg>yki RNAi-1: esg-Gal4, UAS-GFP, Tub-Gal80^TS/+; yki RNAi-1/+) contains fewer Esg(+) cells in response to DSS-induced damage, compared with the wild-type gut (top panel is esg>GFP: w¹¹¹⁸/+; esg-Gal4, UAS-GFP, Tub-Gal80^TS/+). (B) Quantification of mitoses shows that DSS (top) and Pseudomonas (bottom) exposure reduces the regenerative response of ISCs expressing yki RNAi constructs. Error bars indicate s.e.m. (P<0.05). (C) The frequency of Esg(+) cells in the posterior midgut is also reduced, when flies are fed either DSS or Pseudomonas, and Yki is concomitantly depleted. Error bars indicate s.e.m. (P<0.05). (D) Confocal images show a reduction in the size of yki mutant clones (yki^B5) when compared with wild type (arm-LacZ) when the midgut is injured, although both contain ISCs marked by Dl (arrows). (E) After injury, yki mutant clones are smaller than wild type (arm-LacZ). However, under baseline conditions, these are similar in size to wild type. Brackets show total number of clones analyzed at this timepoint (14 days after clone induction), error bars indicate s.e.m. (P<0.05). (F) Confocal images showing the esg>Gal4/ex-LacZ reporter line (esg-Gal4, UAS-GFP, Tub-Gal80^TS/ex-LacZ) under normal conditions and injury conditions. Samples were prepared identically and images were taken using the same parameters.