Fig. 1: Inhibition of the miR-200 family has differential effects during cardiac development. | Nature Communications

Fig. 1: Inhibition of the miR-200 family has differential effects during cardiac development.

From: Single-nuclei multiomics analysis identifies abnormal cardiomyocytes in a murine model of cardiac development

Fig. 1

A Seed sequences of the miR-200a and miR-200c subfamilies. B Genomic location of miR-200a (Blue) and miR-200c (Magenta). miRs located on chromosome (Chr) 4 are intragenic and found in the second intron of Ttl10, while miRs located on chromosome 6 are intergenic. C Cardiac expression of miR-200a and miR-200c at E12.5, E14.5, E16.5, and P28. RNA was isolated from wild-type (WT) whole murine hearts. N = 4. (Shown as Ct values). D E14.5 hematoxylin and eosin stained transverse cardiac sections from Wild-Type, PMIS-A, PMIS-C, and PMIS-AC. The arrowhead shows a ventricular septal defect (VSD) and the arrow shows an atrial septal defect (ASD) in PMIS-AC embryos. RA, Right Atrium; LA, Left Atrium; RV, Right Ventricle; LV, Left Ventricle; VS, Ventral Septum. Corresponding anterior/posterior sections are seen in Supplementary Fig. 2. Scale bar = 100 µm. E Compact left ventricle compact myocardium thickness of WT, PMIS-A, PMIS-C, and PMIS-AC. N = 4. F Western Blot for Mef2c, Tbx5, Gata4, and Pitx2. Protein was isolated from E14.5 whole hearts. Lower panel: Quantification of Mef2c, Tbx5, Gata4 and Pitx2 normalized to Gapdh. N = 3. G Functional testing of miR-200a and miR-200c binding to the Mef2c 3’ UTR. Lower panel: identity of miR binding sequences in the Mef2c 3’UTR. N = 5. The statistic test performed was one-way ANOVAwith multiple comparisons. Data are presented as mean values ± SEM. *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.00001.

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