Fig. 7: SynT-I defects correlate with cardiac pathologies.
From: Defects in placental syncytiotrophoblast cells are a common cause of developmental heart disease
a RT-qPCR analysis of SynT-I marker Slc16a1 (=MCT1) in WT (n = 11), Atp11a- (n = 3), Pparg- (n = 3) and Smg9-mutant (n = 3) TSC clones after 4 days of differentiation. Data are from independent clones each, displayed as mean ± SEM (one-way ANOVA, Holm-Šídák’s multiple comparisons test,* p < 0.05, ** p < 0.01). b Schematic diagram of major TSC differentiation trajectories, highlighting the SynT-I pathway compromised in Atp11a−/−, Pparg−/−, and Smg9−/− TSCs. c Principal component analysis of bulk placental RNA-seq data filtered for SynT-I marker genes39. SynT-I expression patterns separate all KO samples (n = 25) from unaffected WT and HET samples (n = 51). The highlighted datapoint is an Atp11a+/− placenta of an embryo exhibiting VSD; it clusters closer to the KO samples (Fig. 1f). d Diagram depicting the apparent connection between SynT-I differentiation and heart development. Source data are provided as a Source Data file. All exact p-values are provided in Supplementary Data 1.
