Author contributionsS.K., J.A.K., and H.K. derived the RILs and performed the molecular experiments; S.K., J.A.K., and D.H.K. planned the experiments and analyzed the data; S.K. and D.H.K performed transcriptome analysis; D.H.K. supervised and completed the writing.

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SUMMARY Methylglyoxal (MG) is a toxic by‐product of the glycolysis pathway in most living organisms and was previously shown to inhibit seed germination. MG is detoxified by glyoxalase I and II family proteins in plants. MG is abundantly produced during early embryogenesis in Arabidopsis seeds. However, the mechanism that alleviates the toxic effect of MG in maturing seeds is poorly understood. In this study, by T‐DNA mutant population screening, we found that mutations in a glyoxalase I gene (named GERMINATION‐IMPAIRED GLYOXALASE 1, GIG1) led to significantly impaired germination compared with wild‐type seeds. Transformation of full‐length GIG1 cDNA under the constitutively active cauliflower mosaic virus 35S promoter in the gig1 background completely recovered the seed germination phenotype. Quantitative reverse transcription polymerase chain reaction (qRT‐PCR) analyses revealed that GIG1 is uniquely expressed in seeds and is upregulated by abscisic acid (ABA) and downregulated by gibberellic acid (GA) during seed germination. An ABA signaling component, ABI3, directly activated GIG1 in maturing seeds. In addition, PHYTOCHROME INTERACTING FACTOR 1 (PIF1) also plays cooperatively with ABI3 in the regulation of GIG1 expression in the early stage of imbibed seeds. Furthermore, GIG1 expression is stably silenced by epigenetic repressors such as polycomb repressor complexes. Altogether, our results indicate that light and ABA signaling cooperate to enhance seed germination by the upregulation of GIG1 to detoxify MG in maturing seeds.