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.