Fig. 7: Egr is a downstream target of EGFR-MAPK signaling.
From: Inter-cell type interactions that control JNK signaling in the Drosophila intestine
a–d Various genetic manipulations in progenitors driven by esgts (c). 2–3-day-old adult females were shifted from 18 to 29 °C for 2, 3, or 5 days (as indicated in panels) before dissection or infection. Midguts were stained with anti-GFP/-pH3 antibodies. Nuclei were labeled in blue. b ISC mitoses were quantified by counting pH3+ cells. Quantification data represent the mean ± SD (two-tailed unpaired t-test, ****P < 0.0001), with each dot representing one sample. N values indicate the number of midguts examined. Images in (a, c, d) are representative of three independent experiments. Scale bars: 15 μm in (a) and 20 μm in (c, d). e The working model proposed in this paper illustrates a spatial activation pattern of JNK signaling within the intestinal stem cell lineage. Our findings reveal a previously unrecognized Egr/Grnd/JNK-Rho-Krn/Spi-EGFR-Egr pathway that establishes a feedforward loop between ECs and progenitor cells. This feedforward loop could be initiated either by stress-induced downregulation of ALG3 and ALG9 in progenitors or by damage that directly stimulates JNK signaling in ECs. It plays a pivotal role in maintaining Egr production in progenitors and sustaining JNK activation during gut epithelial regeneration. Source data are provided as a Source Data file.
