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. 2021 Dec 9;12:7150. doi: 10.1038/s41467-021-27384-4

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — A Quantification of mitotic numbers after disrupting ISC migration in intestines infected with Ecc15 for 16hrs. B Montage and quantification of ISC migratory behavior after modulating cell cycle progression. OE = overexpression. ISCs outlined in white, and montage tracks measured from the leading edge or, in cells that did not form protrusions, the most distal region of the cell cortex. Mock-treated and Ecc15-infected controls were taken from Fig. 1B, as they served as genetic controls. C Gut length decreases following 24 hrs of Ecc15 infection, but overcompensates after 2 days of recovery. Disrupting ISC migration impairs recovery. D P.e. was fed to 10d females continuously. Disrupting ISC migration decreased survival rates. E A model of non-canonical Wnt signaling-mediated regulation of ISC migration following injury. Mmp1 is activated in EE cells, which, in turn, facilitates activation of the non-canonical Wnt pathway, thereby promoting actin rearrangement. mean ± SEM (A) or mean ± SD (B, C); n = sample size as follows, A: 23 (Control Mock), 16 (Control Ecc15, Dsh RNAi, Otk RNAi), and 18 (Klar RNAi) flies from 2 independent experiments, B: 5 (Control, Wee1 RNAi), 7 (Control Ecc15), and 6 (Wee1 OE) flies from 5 (Control, Control Ecc15), 2 (Wee1 RNAi), and 4 (Wee1 OE) independent experiments, C: 9 (Control, Control 24 hr, Dsh RNAi, Klar RNAi), 10 (Control 2dp), and 8 (Otk RNAi) flies from 2 independent experiments, D: 44 (Control, Dsh RNAi) and 52 (Otk RNAi, Klar RNAi) flies from a single experiment, repeated two independent times with similar trends. **P < 0.01 (C: Control vs Control 24hr = 0.0014), ***P < 0.001 (A, B – Protrusion Formation, B – cell migration: control Ecc15 vs Wee1 OE, C: all except control 2dp vs Otk RNAi < 0.0001, B – Cell Migration: Control vs Wee1 RNAi = 0.0008, C: Control 2dp vs Otk RNAi = .0001), based on one-way ANOVA with Dunnett test (A), two-tailed Student’s t test (B), and one-way ANOVA with Tukey test (C). Individual P values of Fig. 6D = 0.0003 (Control vs Dsh RNAi), < 0.0001 (Control vs Otk RNAi, Control vs Klar RNAi), based on log-rank test (D). Scale bar = 10 µm. Timestamp indicated as hours:minutes. Source data are provided as a Source Data file. See also Supplementary Fig. 7, Supplementary Movies 24–25.