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Figure 1—figure supplement 2. Reprogramming of atrial cardiomyocytes into ventricular cardiomyocytes during development.

(A) Schematic representation of the transgenic lines utilized in lineage tracing experiments. Treatment with 4-hydroxytamoxifen (4-OHT) activates the amhc:CreERT2 protein, which causes the recombination of β-actin2:RSG into β-actin2:GFP, thus permanently labeling amhc expressing cells in green. (B) vmhc:mCherry-NTR; amhc:CreERT2; β-actin2:RSG hearts were exposed to tamoxifen at (C) 3, (D) 4 or (E) 5 dpf in order to genetically label atrial CMs with GFP (c-aGFP), and then confocal imaged at 7 dpf. These hearts that were genetically labeled at (C) 3 (n = 21), (D) 4 (n = 14) or (E) 5 (n = 22) dpf show varying contributions of c-aGFP+ CMs to the ventricles. Green channel – (C’–E’) genetically labeled c-aGFP+ atrial CMs. (F) Quantitation of the percentage of ventricular area covered with c-aGFP+ CMs reveals that although uninjured hearts genetically labeled at 3 and 4 dpf exhibit a small contribution of c-aGFP+ CMs to the ventricle, uninjured hearts labeled at 5 dpf do not. All confocal images shown are maximum intensity projections. V, ventricle; A, atrium; dpf, days post-fertilization. Dashed lines outline the heart. Bars: 50 μm. Mean + s.d. ANOVA test, ***, p<0.001.

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