The biological functions of the epitranscriptomic modification N 6 -methyladenosine (m 6 A) in plants are not fully understood. CPSF30-L is a predominant isoform of the polyadenylation factor CPSF30 and consists of CPSF30-S and an m 6 A-binding YTH domain. Little is known about the biological roles of CPSF30-L and the molecular mechanism underlying its m 6 A-binding function in alternative polyadenylation. Here, we characterized CPSF30-L as an Arabidopsis m 6 A reader whose m 6 A-binding function is required for the floral transition and abscisic acid (ABA) response. We found that the m 6 A-binding activity of CPSF30-L enhances the formation of liquid-like nuclear bodies, where CPSF30-L mainly recognizes m 6 A-modified far-upstream elements to control polyadenylation site choice. Deficiency of CPSF30-L lengthens the 3 0 untranslated region of three phenotypes-related transcripts, thereby accelerating their mRNA degradation and leading to late flowering and ABA hypersensitivity. Collectively, this study uncovers a new molecular mechanism for m 6 A-driven phase separation and polyadenylation in plants.

Similar to epigenetic DNA and histone modifications, epitranscriptomic modifications (RNA modifications) have emerged as crucial regulators in temporal and spatial gene expression during eukaryotic development. To date, over 170 diverse types of chemical modifications have been identified upon RNA nucleobases. Some of these post-synthesized modifications can be reversibly installed, removed, and decoded by their specific cellular components and play critical roles in different biological processes. Accordingly, dysregulation of RNA modification effectors is tightly orchestrated with developmental processes. Here, we particularly focus on three well-studied RNA modifications, including N6-methyladenosine (m6A), 5-methylcytosine (m5C), and N1-methyladenosine (m1A), and summarize recent knowledge of underlying mechanisms and critical roles of these RNA modifications in stem cell fate determination, embryonic development, and cancer progression, providing a better understanding of the whole association between epitranscriptomic regulation and mammalian development.