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The prevalent m 6 Am mRNA cap modification was recently identified as a valid target for removal by the human obesity gene  FTO  along with the previously established m 6 A mRNA modification. However, the deposition and dynamics of m 6 Am in regulating obesity are unknown. Here, we investigate the liver m 6 A/m methylomes in mice fed on a high fat Western-diet and in ob/ob mice. We find that FTO levels are elevated in fat mice, and that genes which lost m 6 Am marking under obesity are overly downregulated, including the two fatty-acid-binding proteins FABP2, and FABP5. Furthermore, the cellular perturbation of  FTO  correspondingly affect protein levels of its targets. Notably, generally m 6 Am- but not m 6 A-methylated genes, are found to be highly enriched in metabolic processes. Finally, we deplete all m 6 A background via  Mettl3  knockout, and unequivocally uncover the association of m 6 Am methylation with increased mRNA stability, translation efficiency, and higher protein expression. Together, these results strongly implicate a dynamic role for m 6 Am in obesity-related translation regulation.

Dynamic regulation of N6,2′-O-dimethyladenosine (m6Am) in obesity