ABI5-activated ALKBH10B demethylates RAP2.6 mRNA to modulate Arabidopsis salt tolerance

Salt stress induces ABI5 → ALKBH10B transcription; the demethylase removes m⁶A from RAP2.6 mRNA, accelerating its decay and attenuating salt-responsive genes, thus linking ABA signaling to reversible m⁶A control of Arabidopsis salt tolerance. N⁶-methyladenosine (m⁶A) is the most prevalent internal modification of RNA and plays an important role in regulating RNA metabolism that governs development and environmental adaptation of plants. Here we dissect how the Arabidopsis m⁶A demethylase ALKBH10B is integrated into abscisic-acid (ABA)-mediated salt-stress signaling. Under salt treatment, loss of ALKBH10B exhibited significantly delayed seed germination. Salt stress could significantly induce the expression of ALKBH10B transcription via the ABA-responsive transcription factor ABI5, which binds directly bind to the ABRE element in the ALKBH10B promoter and activate its transcription. Multi-omic integration of m⁶A methylomes and transcriptome identified the AP2/ERF transcription factor RAP2.6 as a direct target of ALKBH10B. ALKBH10B removed m⁶A modifications on RAP2.6 mRNA, accelerating its degradation and modulating the expression of salt-responsive genes. In summary, this study elucidates the salt stress response pathway ABI5-ALKBH10B-RAP2.6 that couples ABA perception to reversible m⁶A modification, providing mechanistic insight into the intricate regulatory network of dynamic m⁶A modifications in plant stress adaptation.