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. 2019 May 20;49(4):556–573.e6. doi: 10.1016/j.devcel.2019.04.033

Figure 3.

Figure 3

Kismet Controls Proliferation by Regulating EGFR Pathway Activity

(A–D′) Wild-type (A, A′, C, and C′) and kis10D26 (B, B′, D, and D′), 9 days AHS MARCM clones. EGFR signaling, detected by dpERK (A–B′) and EGFR target CycE-LacZ (C–D′), was increased in kis10D26 clones.

(E–F′) Wild-type (E and E′), and kis10D26 (F and F′), 3 days AHS MARCM clones expressing CycE-LacZ.

(G) Proportion of ISCs expressing CycE-lacZ from (E) and (F′).

(H and I) ISC-specific expression of GFP (H) or kis RNAi (BL34908) (I), 3 days at 29°C.

(J) Quantification of proportion of ISCs showing strong, weak, or no dpERK from (H)–(I′).

(K–N) 12-day AHS clones: wild-type (K), kis10D26 mutant (L), expressing UAS-EGFRDN (M), and kis10D26 mutant expressing UAS-EGFRDN (N).

(O) Clone size, number of Delta+ cells/clone, and % of Delta+ cells/clone from (K)–(N).

(P and Q) 10-day AHS clones: wild-type expressing cic (P) and kis10D26 mutant expressing cic (Q).

(R) Clone size, number of Delta+ cells/clone, and % of Delta+ cells/clone from (P) and (Q).

Results compared using a chi-square test in (G) and (J) and a two-tailed Mann-Whitney test in (O) and (R). Mean values in red; error bars, SEM; ns = non-significant, **p < 0.01, ****p > 0.0001. Arrows highlight ISCs. Scale bars, 20 μm.