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. 2020 Oct 20;11:5300. doi: 10.1038/s41467-020-19150-9

Fig. 1. Defective contribution of Cx40+ derived trabecular cells to the postnatal PF in Nkx2-5+/− mice.

Fig. 1

a Scheme of the strategy used for genetic lineage tracing of Cx40+ cells. R26R-YFP reporter mouse line are crossed with tamoxifen inducible Cx40-CreERT2 mice. Injection of tamoxifen induces the recombination of loxP sites resulting in the expression of the fluorescent protein YFP in Cx40+ cells. b Tamoxifen is injected at E14 and Cx40+ derivative cells are analyzed at P7. c Immunostaining for YFP and RFP on Cx40-CreERT2-RFP::R26R-YFP control (ctrl) or Nkx2-5+/− heart transverse sections at P7, shows distribution of Cx40+ derivative cells (YFP+) and their fate into PFs (YFP+RFP+). Asterisks represent papillary muscles; scale bars = 200 µm. (n = 4 Ctrl and Nkx2-5+/−). d–f Graphs of quantifications from c images. The total number PF cells (RFP+) per section d, the total number of trabecular-derived cells (YFP+) e, and the relative contribution of trabecular cells to PFs ((YFP+RFP+)/YFP+) f are quantified in mid and apical sections. Box plots show the median, the 25th and 75th percentile, and the whiskers denote the minimum and maximum values, respectively. Mean of 3 sections/heart; (n = 4 Ctrl and Nkx2-5+/−). P values are derived ordinary one-way ANOVA test, *P < 0.05; ***P < 0.001. g Scheme illustrating the differentiation of embryonic trabecular progenitors into conductive and contractile cardiomyocytes. In Nkx2-5+/− mice, the cell fate decision into conductive cardiomyocytes is disturbed and haploinsufficient trabecular progenitors mostly give rise to contractile cardiomyocytes.