Figure 6. Pe ingestion induces ISC proliferation.

(A) Stat92E, Dome, or Notch were depleted from progenitor cells by UAS-RNAi using esg^ts, 2d prior to Pe infection. hep¹ is a hypomorphic JNKK allele. JNK signaling was also downregulated in ECs by expressing UAS-Puc using MyoIA^ts. Midguts were scored for PH3⁺ mitotic figures 2d after infection (green). “Mock” indicates control animals shifted to food without Pe.

(B) Midgut mRNAs measured in WT by RT-qPCR, 2d after Pe infection (red) or in controls (green). The data were normalized to day 0 (before infection) samples.

(C) Midgut mRNAs measured in MyoIA^ts>Puc animals by RT-qPCR, 2d after Pe infection. The data were normalized to mock infected controls.

(D) Quantification of Delta⁺ ISCs, MyoIA>GFP⁺ ECs and pros⁺ EEs during gut regeneration induced by Pe.

(E-L) Reporter expression in midguts 2 days after mock (E, G, I and K) or Pe (F, H, J and L) infection.

(E, F) A low level of the JNK reporter, puclacZ, was observed in ECs and EEs (usually paired, arrowheads) in controls (E). Widespread puclacZ after Pe infection (F). puclacZ was not expressed in progenitor cells (arrows).

(G, H) updlacZ was not expressed in controls (G), but was induced in progenitor cells or pre-ECs after Pe infection (H).

(I, J) upd3Gal4-driven GFP in controls (I), or after Pe infection (J).

(K, L) The Stat reporter, 10XSTAT-DGFP, was normally confined to progenitor cells (K), but was present in many cells after Pe infection (L). Blue: DNA in all panels.