The m6A-modified ApMETTL13 participates in light-dependent growth regulation in the dinoflagellate Alexandrium pacificum

Red tides pose a serious threat to ecological security and human health, making it critical to understand the proliferation mechanisms of toxic dinoflagellates such as Alexandrium pacificum . Given the limited transcriptional regulation in dinoflagellates, post-transcriptional mechanisms such as N6-methyladenosine (m6A) are likely key regulators. This study investigated the function of m6A in A. pacificum growth regulation. Treatment with the m6A inhibitor STM2457 significantly reduced overall m6A levels, which in turn suppressed algal cell growth and photosynthesis. To uncover the underlying molecular cascade, combined MeRIP-seq and RNA-seq analysis under different light intensities (200 vs 30 μmol photons/(m 2 ·s)) was performed. Among 307 differentially m6A-modified genes, ApMETTL13 was identified as the top candidate, exhibiting the most pronounced increase in m6A modification and transcript expression; these results were validated by MeRIP-qPCR and RT-qPCR. Functional prediction and molecular docking suggested that ApMETTL13 may methylate lysine 55 of eukaryotic elongation factor 1A in A. pacificum (ApeEF1A), thereby regulating its activity. Further experiments indicated that, under high light, ApMETTL13 -mediated m6A modification may promote K55me2 modification on ApeEF1A, potentially influencing the cell cycle and facilitating rapid algal growth. These findings reveal a potential epigenetic transcriptome-driven regulatory cascade, from RNA modification to protein expression, enzyme activity, and substrate modification, that may govern light-dependent growth in A. pacificum . The results provide precise data and potential targets for understanding dinoflagellate red tide dynamics and advance the functional knowledge of m6A modifications in marine algae.