FLK is an mRNA mA reader that regulates floral transition by modulating the stability and splicing of FLC in Arabidopsis.

N-methyladenosine (mA), which is added, removed, and interpreted by mA writers, erasers, and readers, respectively, is the most abundant modification in eukaryotic mRNAs. The mA 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 mA reader protein that directly binds the mA 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 mA writer mutant, and the late-flowering phenotype of the flk mutant could not be rescued by genetic complementation using the mutant FLK gene, in which the mA reader encoding function was eliminated, indicating that FLK binds and regulates FLC expression in an mA-dependent manner. Collectively, our study has addressed a long-standing question of how FLK regulates FLC transcript levels and established a molecular link between the FLK-mediated recognition of mA modifications on FLC transcripts and floral transition in Arabidopsis.