ABI4-HDA9 Module Epigenetically Silences GIG1 to Accumulate Methylglyoxal for Seed Thermoinhibition Response in Arabidopsis thaliana.

Methylglyoxal (MG) as a toxic by-product of the glycolysis pathway, gradually accumulates to delay seed germination, while glyoxalases efficiently detoxify MG to initiate seed germination. GIG1 encoding a seed-specific glyoxalase is required for light-induced seed germination. Supraoptimal temperature (SOT) triggers seed secondary dormancy, termed as seed thermoinhibition, thereby avoiding seed germination under unfavourable conditions. In this study, we demonstrated that SOT suppressed the expression of GIG1 and glyoxalase activity, leading to rapid MG accumulation during seed thermoinhibition response. Consistently, overexpressing GIG1 enhanced seed germination, while gig1 mutant displayed lower seed germination under SOT stress, suggesting that MG signal regulates seed thermoinhibition response via suppressing GIG1 expression to dampen glyoxalase activity. Mechanistically, SOT-induced ABI4, an essential component of Abscisic Acid (ABA) signalling, and recognised the CCAC motif within the promoter of GIG1 to suppress the expression of GIG1; During this process, ABI4 recruited HDA9 to epigenetically silence GIG1 expression by histone deacetylation modification at GIG1 locus. Collectively, our results demonstrate the novel function of MG signalling in triggering seed thermoinhibition response, and propose that the ABI4-HDA9 module coordinates MG content by epigenetically modulating GIG1 expression and glyoxalase enzyme activity during seed thermoinhibition process.