摘要N6-methyladenosine(m6A),which is added,removed,and interpreted by m6A writers,erasers,and readers,respectively,is the most abundant modification in eukaryotic mRNAs.The m6A marks play a pivotal role in the regulation of floral transition in plants.FLOWERING LOCUS K(FLK),an RNA-binding protein harboring K-homology(KH)motifs,is known to regulate floral transition by repressing the levels of a key floral repressor FLOWERING LOCUS C(FLC)in Arabidopsis.However,the molecular mechanism underlying FLK-mediated FLC regulation remains unclear.In this study,we identified FLK as a novel mRNA m6A reader protein that directly binds the m6A site in the 3'-untranslated region of FLC transcripts to repressing FLC levels by reducing its stability and splicing.Importantly,FLK binding of FLC transcripts was abolished in vir-1,an m6A writer mutant,and the late-flowering phenotype of the flk mutant could not be rescued by ge-netic complementation using the mutant FLKm gene,in which the m6A reader encoding function was elim-inated,indicating that FLK binds and regulates FLC expression in an m6A-dependent manner.Collectively,our study has addressed a long-standing question of how FLK regulates FLC transcript levels and estab-lished a molecular link between the FLK-mediated recognition of m6A modifications on FLC transcripts and floral transition in Arabidopsis.