N6-methyladenosine (m6A) reader Pho92 is directed by Paf1C to meiotic mRNAs in an m6A-dependent and independent manner and promotes CCR4-NOT-mediated mRNA decay of m6A modified transcripts contingent on translation.

Inhibiting RNA N6-methyladenosine demethylase ALKBH5 promoted axonal regeneration of dorsal root ganglion neurons by regulating stability of Lpin2 mRNA and enhanced the survival and axonal regeneration of retinal ganglion cells.

YTHDC1 facilitates selective clearance of N6-methyladenosine methylated mRNAs from the nucleus to the cytoplasm through binding by nuclear 'reader' proteins and incorporation into the canonical mRNA export pathway.

METTL3 and m6A modifications could alleviate endothelial activation and atherogenesis through accelerated degradation of oscillatory flow-induced EGFR mRNA expression.

Human proteins that add or remove the methyladenosine modification of cellular RNA, or recognize methylated RNA significantly affect HIV-1 infection or viral protein synthesis in cells, suggesting an important role for HIV-1 RNA methylation in regulating viral replication.

SND1 has m6A-reading ability and is essential for Kaposi's sarcoma-associated lytic replication.

The N6-methyladenosine (m6A) methyltransferase complex in budding yeast is highly conserved, yet reconfigured with respect to its mammalian counterpart and has both m6A-dependent and m6A-independent functions.

Purine recycling deficiency triggers metabolic and neurological defects reminiscent of Lesch–Nyhan disease in Drosophila, paving the way for studying this disorder and carrying out drug screening in an invertebrate organism.

Biochemical, molecular, and genetic analyses show that in Drosophila the epigenetic enzyme TET does not demethylate 6mA, which is scarce in the genome, but rather acts in a catalytic-independent manner.