FLK is an mRNA m6A reader that regulates floral transition by modulating the stability and splicing of FLC in Arabidopsis

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 3MODIFIER LETTER PRIME-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.

Automated summary

N6-methyladenosine (m6A) is the most abundant modification in eukaryotic mRNAs and is regulated by m6A writers, erasers, and readers. The study identified FLK as a novel mRNA m6A reader protein that directly binds the m6A site in the FLC transcripts to repress FLC levels. This finding establishes a molecular link between FLK-mediated recognition of m6A modifications and floral transition in Arabidopsis.