Fig. 7: Nkx2.5 regulates targets, ect2, psmb3, and psmd7, to orchestrate regenerative mechanisms.
From: Activation of Nkx2.5 transcriptional program is required for adult myocardial repair

A, B Representative images of RNAscope analysis on sections of injured hearts at 7 dpa display decreased ect2 expression in the regenerating myocardium of the nkx2.5−/− (n = 7) (B) compared to the non-transgenic wild-type (n = 3) (A) fish. Dashed lines represent amputation planes. Scale bar, 50 μm. C, D Additional RNAscope analysis employing both nkx2.5 and ect2 probes simultaneously highlight co-localization of transcripts in individual nuclei at the injury border zone in non-transgenic wild-type fish (n = 3) (C). Higher magnification panel (D) indicates the area outlined in the rectangular box. Scale bar, 50 μm. E–H In situ hybridization for psmb3 (E, F) and psmd7 (G, H) in non-transgenic wild-type (n = 5) (E, G) and nkx2.5−/− (n = 5) (F, H) adult hearts. In nkx2.5−/− hearts, both psmb3 and psmd7 are downregulated in the injured area. Scale bar, 30 μm. I, J Quantification of psmb3 (I) and psmd7 (J) signal, detected by in situ hybridization, reveals statistically significant diminution of both genes in the nkx2.5−/− (n = 5) compared with the wild-type (n = 5) injured myocardium. Mean and standard error of each data set are shown. Unpaired, two-tailed t-test illustrate statistically significant differences in (I) (p = 0.0297) and (J) (p = 0.0468). Source data are provided as a Source Data file.