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However, the role of m\n                    <jats:sup>6<\/jats:sup>\n                    A in heart regeneration remains largely unclear. To study m\n                    <jats:sup>6<\/jats:sup>\n                    A function in heart regeneration, we modulated Mettl3 expression in vitro and in vivo. Knockdown of\n                    <jats:italic>Mettl3<\/jats:italic>\n                    significantly increased the proliferation of cardiomyocytes and accelerated heart regeneration following heart injury in neonatal and adult mice. However,\n                    <jats:italic>Mettl3<\/jats:italic>\n                    overexpression decreased cardiomyocyte proliferation and suppressed heart regeneration in postnatal mice. Conjoint analysis of methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA-seq identified\n                    <jats:italic>Fgf16<\/jats:italic>\n                    as a downstream target of Mettl3-mediated m\n                    <jats:sup>6<\/jats:sup>\n                    A modification during postnatal heart regeneration. RIP-qPCR and luciferase reporter assays revealed that Mettl3 negatively regulates\n                    <jats:italic>Fgf16<\/jats:italic>\n                    mRNA expression in an m\n                    <jats:sup>6<\/jats:sup>\n                    A-Ythdf2-dependent manner. The silencing of\n                    <jats:italic>Fgf16<\/jats:italic>\n                    suppressed the proliferation of cardiomyocytes. However, the overexpression of \u0394Fgf16, in which the m\n                    <jats:sup>6<\/jats:sup>\n                    A consensus sequence was mutated, significantly increased cardiomyocyte proliferation and accelerated heart regeneration in postnatal mice compared with wild-type Fgf16. Our data demonstrate that Mettl3 post-transcriptionally reduces\n                    <jats:italic>Fgf16<\/jats:italic>\n                    mRNA levels through an m\n                    <jats:sup>6<\/jats:sup>\n                    A-Ythdf2-dependen pathway, thereby controlling cardiomyocyte proliferation and heart regeneration.\n                  <\/jats:p>","DOI":"10.7554\/elife.77014","type":"journal-article","created":{"date-parts":[[2022,10,18]],"date-time":"2022-10-18T02:15:11Z","timestamp":1666059311000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.77014","source":"Crossref","is-referenced-by-count":44,"title":["Mettl3-mediated m6A modification of Fgf16 restricts cardiomyocyte proliferation during heart regeneration"],"prefix":"10.7554","volume":"11","author":[{"given":"Fu-Qing","family":"Jiang","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02xe5ns62","id-type":"ROR","asserted-by":"publisher"}],"name":"Key Laboratory of Regenerative Medicine of Ministry 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