Specifically recognizes and binds N6-methyladenosine (m6A) -containing RNAs, and regulates their stability. M6A is amodification present at internal sites of mRNAs and some non-codingRNAs and plays a role in mRNA stability and processing. Acts as a regulator of mRNA stability by promotingdegradation of m6A-containing mRNAs via interaction with the CCR4-NOTand ribonuclease P/MRP complexes, depending on the context. The YTHDF paralogs (YTHDF1, YTHDF2 and YTHDF3) sharem6A-containing mRNAs targets and act redundantly to mediate mRNAdegradation and cellular differentiation. M6A-containing mRNAs containing a binding site forRIDA/HRSP12 (5'-GGUUC-3') are preferentially degraded byendoribonucleolytic cleavage: cooperative binding of RIDA/HRSP12 andYTHDF2 to transcripts leads to recruitment of the ribonuclease P/MRPcomplex. Other m6A-containing mRNAs undergodeadenylation via direct interaction between YTHDF2 and CNOT1, leadingto recruitment of the CCR4-NOT and subsequent deadenylation of m6A-containing mRNAs. Required maternally to regulateoocyte maturation: probably acts by binding to m6A-containing mRNAs, thereby regulating maternal transcript dosage during oocyte maturation, which is essential for the competence of oocytes to sustain earlyzygotic development. Also required duringspermatogenesis: regulates spermagonial adhesion by promotingdegradation of m6A-containing transcripts coding for matrixmetallopeptidases. Also involved in hematopoietic stemcells specification by binding to m6A-containing mRNAs, leading topromote their degradation. Also acts as a regulatorof neural development by promoting m6A-dependent degradation of neuraldevelopment-related mRNA targets. Inhibits neuralspecification of induced pluripotent stem cells by binding tomethylated neural-specific mRNAs and promoting their degradation, thereby restraining neural differentiation. Regulatescircadian regulation of hepatic lipid metabolism: acts by promotingm6A-dependent degradation of PPARA transcripts. Regulates the innate immune response to infection by inhibiting thetype I interferon response: acts by binding to m6A-containing IFNBtranscripts and promoting their degradation. May alsoact as a promoter of cap-independent mRNA translation following heatshock stress: upon stress, relocalizes to the nucleus and specificallybinds mRNAs with some m6A methylation mark at their 5'-UTR, protectingdemethylation of mRNAs by FTO, thereby promoting cap-independent mRNAtranslation. Regulates mitotic entry by promoting thephase-specific m6A-dependent degradation of WEE1 transcripts. Promotes formation of phase-separated membranelesscompartments, such as P-bodies or stress granules, by undergoingliquid-liquid phase separation upon binding to mRNAs containingmultiple m6A-modified residues: polymethylated mRNAs act as amultivalent scaffold for the binding of YTHDF proteins, juxtaposingtheir disordered regions and thereby leading to phase separation. The resulting mRNA-YTHDF complexes then partition into differentendogenous phase-separated membraneless compartments, such as P-bodies, stress granules or neuronal RNA granules. May alsorecognize and bind RNAs modified by C5-methylcytosine (m5C) and act asa regulator of rRNA processing. [1-10]

MSASSLLEQRPKGQGNKVQNGSVHQKDGLNDDDFEPYLSPQARPNNAYTAMSDSYLPSYYSPSIGFSYSLGEAAWSTGGDTAMPYLTSYGQLSNGEPHFLPDAMFGQPGALGSTPFLGQHGFNFFPSGIDFSAWGNNSSQGQSTQSSGYSSNYAYAPSSLGGAMIDGQSAFANETLNKAPGMNTIDQGMAALKLGSTEVASNVPKVVGSAVGSGSITSNIVASNSLPPATIAPPKPASWADIASKPAKQQPKLKTKNGIAGSSLPPPPIKHNMDIGTWDNKGPVAKAPSQALVQNIGQPTQGSPQPVGQQANNSPPVAQASVGQQTQPLPPPPPQPAQLSVQQQAAQPTRWVAPRNRGSGFGHNGVDGNGVGQSQAGSGSTPSEPHPVLEKLRSINNYNPKDFDWNLKHGRVFIIKSYSEDDIHRSIKYNIWCSTEHGNKRLDAAYRSMNGKGPVYLLFSVNGSGHFCGVAEMKSAVDYNTCAGVWSQDKWKGRFDVRWIFVKDVPNSQLRHIRLENNENKPVTNSRDTQEVPLEKAKQVLKIIASYKHTTSIFDDFSHYEKRQEEEESVKKERQGRGK