Figure 1. Enteroendocrine fate choice does not relies on a negative feedback loop from the differentiated enteroendocrine cells.

• A–F
  (A, C, E) Adult posterior midguts containing control clones, those lacking EEs, or with extra EEs (clones outlined), observed 10 days after heat shock (AHS). Images are compiled tile scans stitched together in Zen software. In (A, C), we used a modified MARCM technique in which ProsGal4 was clonally activated when GAL80 was clonally lost through FLP/FRT‐mediated mitotic recombination. Clones were detected by the loss of RFP baring Gal80 chromosome. Scale bar = 100 μm. (A) Control wild‐type clones marked by lack of RFP expression, DNA in blue, and EE cells marked by Pros in green. (B) Schematic view of (A) with EE cells represented in red and clone delineated in black and shown in white. (C) EE depletion by clonal expression of rpr under the control of prosGal4 using the GAL80 system in negatively marked clones (lacking RFP expression and GAL80 expression). (D) Scheme of (C). (E) EE accumulation in MARCM clones (green) expressing RNAi against Notch. DAPI in blue, EE cells marked through Pros, in red. (F) Scheme of (E).
• G
  Global EE density measured in clonal and non‐clonal compartments in control wild‐type clones, upon EE depletion and ectopic EE cells. The bars represent mean values ± SD.
• H, I
  Number of EE cells located in a 30‐μm‐wide band around each individual clone normalized by clonal area (H) and clonal perimeter (I). The bars represent mean values ± SEM.

Data information: Results were compared using a two‐tailed Mann–Whitney statistical test (ns = non‐significant, P‐values indicated).