SMAX1 interacts with DELLA protein to inhibit seed germination under weak light conditions via gibberellin biosynthesis in Arabidopsis.

Karrikins (KARs) were first identified as a class of small-molecule chemicals derived from smoke that promote seed germination. However, the implied mechanism is still not well understood. Here, we find that KAR signaling mutants have a lower germination percentage than that of wild type under weak light conditions, and KARs promote seed germination through transcriptional activation of gibberellin (GA) biosynthesis via SMAX1. SMAX1 interacts with the DELLA proteins REPRESSOR of ga1-3 -LIKE 1 (RGL1) and RGL3. The interaction enhances the transcriptional activity of SMAX1 and inhibits GIBBERELLIN 3-oxidase 2 (GA3ox2) gene expression. The KAR signaling mutant seed germination defect under weak light is partially rescued by exogenous application of GA 3 or by GA3ox2 overexpression, and the rgl1 rgl3 smax1 triple mutant exhibits higher germination rates under weak light than the smax1 mutant. Thus, we show a crosstalk between KAR and GA signaling pathways via a SMAX1-DELLA module in regulating seed germination in Arabidopsis. [Display omitted] • KAR signaling mutants have lower germination percentage under weak light • SMAX1 functions as an auto-regulated transcription factor • The interactions of SMAX1 with DELLA proteins regulate SMAX1 transcriptional activity • SMAX1 can inhibit the GA3ox2 gene expression, which is a key enzyme in GA biosynthesis Xu et al. show that KAR signaling protein SMAX1 inhibits seed germination under weak light conditions by regulating gibberellin (GA) biosynthesis. SMAX1 inhibits GA3ox2 gene expression and DELLA proteins interact with SMAX1 to regulate its transcriptional activity, indicating a crosstalk between KAR and GA signaling in regulating Arabidopsis seed germination. [ABSTRACT FROM AUTHOR]