Fig. 3: DBSA relieves ABA-induced inhibition of seed germination and seedling growth, and does not induce ABA-responsive gene expression in Arabidopsis thaliana.

a Germination rate of seeds exposed to ABA (1 µM), DBSA (1 µM) or ABA and DBSA (1 µM:1 µM). DMSO (0.05%) was used as a control. PYL dimer quadruple deletion mutant (pyr1/pyl1/pyl2/pyl4, 1124), PYL monomer multiple deletion mutant (pyl3/pyl7/pyl9/pyl11/pyl12, 3791112), PYL4 overexpression (4OE) seeds are considered germinated when green cotyledons expand (n = 3 biologically replicates). b Seeding growth of WT and 1124 seeds under the treatment of ABA (1 µM), DBSA (1 µM) or ABA and DBSA (1 µM:1 µM). n = 3 biologically replicates. c DBSA and ABA treatment caused different gene expression patterns. d The transcript levels of the common DBSA- and ABA-responsive genes were poorly correlated. The scatter plot shows the log2-transformed expression levels of DBSA-responsive DEGs (y-axis) and ABA-responsive DEGs (x-axis) relative to the DMSO control. e The representative GO terms and pathways enriched in ABA-specific response and DBSA-specific response DEGs based on functional enrichment analysis (p < 0.01). f Induction of abiotic stress marker genes in Arabidopsis thaliana (Col-0) after ABA or DBSA treatment as determined by qRT-PCR. Ten-day-old seedlings were treated with 10 μM ABA or 100 μM DBSA or 10 μM ABA and 100 μM DBSA for 6 h before RNA extraction, and 0.05% DMSO was used as control (n = 3 biologically replicates). For a and f, the data are presented as the mean ± SD, the line within the box marks the median and the whiskers represent the minimum and maximum values. For f, P values are indicated by two-tailed Student’s t test. Source data are provided as a Source Data file.