Fig. 4: The BAM1–GHR1–CLE5p module functions in drought response.
From: Local peptide signalling induces stomatal closure under drought stress

a Images of wild type, bam1-3, ghr1, bam1-3ghr1, and bam1-3ghr1cle5-1 leaves detached for 1.5 h. Scale bar: 1 cm. b Endogenous ABA level in wild type, cle5-1, and bam1-3ghr1 shoots after 2.5 h dehydration stress. Different letters above the columns represent a two-way ANOVA analysis followed by a Tukey Honest Significant Differences test; Pr( > F) for the treatment = 1.8e-08, Pr( > F) for the genotype = 0.695, Pr( > F) for the treatment:genotype interaction = 0.977. DW: dry weight. c Ten-day-old wild type and srk2e seedlings were exposed to drought stress for 20 min, and 20 µg of their crude extracts were subjected to an in-gel kinase reaction with histone III as the substrate. d Short-term application of 1 μM [Ara3]CLE5p to wild type, srk2e, and nced3 leaves for 30 min. Left: representative images of stomata. Scale bars, 5 μm. Right: statistics of stomatal aperture, measured as the ratio of pore width to length (W/L). e qRT-PCR analysis of RD29B and RAB18 (drought stress-responsive genes) expression in wild type and ABA-insensitive (abi1-1) seedlings treated with Mock or 1 μM [Ara3]CLE5p for 1 h. f Schematic representation of the BAM1–GHR1–CLE5p/SRK2E signal transduction module. Upon drought stress, CLE5p is captured by the BAM1–GHR1 receptor complex, located on the plasma membrane of guard cells. This module phosphorylates SRK2E and SRK2D kinases to induce stomatal closure and activate the expression of drought stress-responsive genes without stimulating the canonical ABA pathway. Biological replicates (N) and sample size per replicate (n) for (b, c, and e) are listed in Supplementary Data 4; P values in (c, e) were calculated with two-tailed unpaired t-test; the experiments in a and e were repeated three times, with similar results. n.s., not significant. See also Supplementary Fig. 10.