Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 May 22;10:2267. doi: 10.1038/s41467-019-09929-w

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 5 — Epigenetic modulation of SCN5A gene expression. a, b ChIP analyses in CNTR-CMs and K219T-CMs with antibodies against Lamin A/C (a) and H3K27me3 (b) targeting the SCN5A genomic region. Data are presented as a percentage of input chromatin precipitated and relative to 2 independent iPSC clones from each subject. ChIP for Lamin A/C, indicating increased binding of Lamin A/C to the promoter region of the SCN5A gene in K219T-CMs; no enrichment was detectable for JUN, used as a negative control region for the ChIP experiment; SCN10A, DEFA3, and DEFA4 were used as positive control regions for the ChIP experiments, and they show comparable enrichment of Lamin A/C in CNTR-CMs and K219T-CMs (a). ChIP for the histone modification H3K27me3, showing an enrichment of the repressive histone mark at the SCN5A gene promoter in K219T-CMs, supporting the reduced expression of the gene detected in these cells; NEURO D was used as positive control region for the antibody (b). c ChIP against Lamin A/C, showing the dynamics of Lamin A/C enrichment at the transcription start site (TSS) of SCN5A during cardiac differentiation (from days 0 to 12). The graph is relative to one representative experiment (out of three). For this analysis, two-way ANOVA was used for the statistic test. **p < 0.01. d 3D-FISH for Lamin A/C (green) and SCN5A (magenta) conducted with an antibody and a DNA probe, respectively. Left: representative images of nuclei from CNTR and K219T-CM preparations (Scale bar: 9 μm). Magnified box shows the colocalization of the SCN5A probe at the nuclear lamina. Right: Analysis of the distance from the nuclear lamina, showing preferential localization of the SCN5A probe (magenta) at the nuclear periphery in K219T-CMs vs. CNTR. Quantification was carried out using a specific plug-in of the ImageJ software (CNTR-CMs: n = 72 cells; K219T-CMs: n = 82 cells; p < 0.0001). All values are reported as means ± SD, if not differently specified. *p < 0.05; **p < 0.01, ns, not significant (unpaired t-test)