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Fig. 1 - Supplemental 3 Synergy between a reprogramming factor and KRASG12V oncogene efficiently induces tumors in zebrafish larvae. (A) Images of control zebrafish larvae at 6 days post-fertilization (dpf): without any treatment (left), with transient incubation in caged cyclofen (cCYC) (without UV, middle) and with incubation in dexamethasone (DEX)+cCYC (without UV, right). Note that zebrafish does show neither morphological anomalies nor mortality. (B) Global photoactivation (via cCYC uncaging with 5 min UV illumination and Cre-ERT activation) of KRASG12V (blue nuclei) in 1 dpf zebrafish without (left) or with subsequent transient activation (right) of Ventx-GR by DEX (described in Figure 2). These larvae (labeled as KR+VX) develop hyperplasic tissues within 6?9 dpf (dorsal view, red arrows indicate hyperplasia). Global photoactivation (via cCYC uncaging and Cre-ERT activation) of KRASG12V (blue nuclei) in 1 dpf zebrafish with subsequent transient activation of NANOG-GR or POU5/OCT4-GR by DEX (setup described in A). These larvae (labeled as KR+NANOG or KR+POU5/OCT4) develop hyperplasic tissues within 6?9 dpf (dorsal view, red arrows indicate hyperplasia). (C) Quantification of zebrafish developing abnormal hyperplasia upon the indicated treatments. Note that only the synergy between reprogramming factors (i.e. VENTX, NANOG, or POU5/OCT4) and the KRASG12V oncogene reproducibly and efficiently induce tumors in zebrafish larvae. The total number of zebrafish larvae analyzed are indicated above the bars. ? indicates no event (0%). Note that in all pictures the asterisk (*) indicates the eye. Scale bars and body axes (a: anterior; p: posterior; d: dorsal; v: ventral; l: left; r: right) are shown.