Fig. 5

Wnt/β-catenin and mTORC1 are active in regenerating mouse and human cardiomyocytes

(A) Heatmap of significantly different amino acids and TCA cycle intermediates in mouse hearts.

(B) Abundance of glutamine in mouse hearts. ∗p < 0.05 versus control, one-way ANOVA performed. N = 2–4 biological replicates.

(C) Heatmap of Wnt ligands and targets in mouse hearts.

(D) Schematic of stem-cell-derived cardiomyocyte (hPSC-CM) generation.

(E) Purity of cardiomyocytes after Wnt activation, inhibition, and/or mTORC1 inhibition as determined by FACs. One-way ANOVA performed. N = 3 biological replicates.

(F) Percentage of proliferating hESC-CMs after Wnt activation, inhibition, and/or mTORC1 inhibition as determined by FACs. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, one-way ANOVA performed. N = 3 biological replicates.

(G) Protein analysis of hPSC-CMs after Wnt activation, inhibition, and/or mTORC1 inhibition.

(H) Protein analysis of hPSC-CMs mTORC1 activation after glutamine transporter inhibition via GPNA. N = 3 biological replicates.

(I) Quantification of p-S6/S6 blots in (H). ∗p < 0.05, two-tailed t test performed.

(J) Schematic of amino acid primed proregenerative cardiomyocyte and the signaling cascade that Wnt/β-catenin drives to turn on mTORC1, Lin28, and Myc to bring about zebrafish heart regeneration. Bar graphs show individual data points with error bars representing standard error of the mean. Source data are provided as a Data S2.