Mettl3-dependent m6A modification regulates heart regeneration by modulating Fgf16 expression in mice

N6-methyladenosine (m6A) methylation, catalyzed by the enzyme methyltransferase-like 3 (Mettl3), is the most prevalent posttranscriptional modification in mRNA. Despite the functional importance of m6A in various physiological and pathological bioprocesses, the function of m6A in heart regeneration remains unclear. It has been demonstrated that complete cardiac regeneration occurs in neonatal mouse heart after ventricular resection at postnatal day 1 (p1), but this capacity is lost at p7, suggesting that regenerative potential is gradually lost during mouse heart development and maturation.For total RNA isolation, neonatal mice were subjected to cardiac apical resection at postnatal day 3 (p3). Heartswere then extracted in sham and injured neonatal mice at 5 days post-resection (dpr), respectively. Three hearts per group were used for RNA-sequencing analysis. RNA preparation, library construction and sequencing on GBISEQ-500 platform was performed as previously described.