Fig. 6: TMEM11 mediates m⁷G methylation of Atf5 and its expression.

a MeRIP-qPCR validation of m⁷G modification levels of genes which selected from the results of MeRIP-seq and mRNA-seq data in TMEM11 Tg and WT mice hearts (n = 6 mice per group). b Expression levels of Atf5 mRNA and protein in WT and TMEM11 Tg mice hearts (n = 6 mice per group). c Integrative Genomics Viewer (IGV) tracks showing MeRIP-seq (upper panel) and mRNA-seq (bottom panel) read distribution in Atf5 mRNA from TMEM11 Tg and WT mice hearts. d MeRIP-qPCR analysis in TMEM11 KO and WT mice hearts shows the m⁷G modification level in Atf5 mRNA (n = 6 mice per group). e Expression levels of ATF5 protein (upper panel) and mRNA (lower panel) in TMEM11 KO and WT mice hearts (n = 6 mice per group). f Neonatal cardiomyocytes were infected with adenovirus harboring TMEM11, and transfected with si-NC or si-ATF5 for 48 h. Qualification of pH3-positive cardiomyocytes was calculated (n = 5 independent experiments). g Knockdown of ATF5 promotes cardiomyocyte proliferation following MI injury. AAV9 loaded with ATF5 shRNA (sh-ATF5) or its control (sh-CTRL) was administered to adult WT mice and subjected to MI, and heart samples were collected at 8 weeks post-MI. Representative confocal images and qualification of pH3-positive cardiomyocytes in heart sections at 8 weeks post-MI (Bar = 25 μm) (n = 6 mice per group). Data are presented as the mean ± s.d. One-way ANOVA (f and g) or two-sided Student’s t test (a, b, d and e) was performed.