Fig. 6: ACL1 recruits TOPLESS to repress ROCs in the regulation of wax content and bulliform cells to synergistically modulate drought tolerance and BPH resistance.

a Y2H of ACL1 interacting with the N-terminals of three TPRs. b LCI assay of ACL1 interacting with the N-terminals of three TPRs. c Expression of BDG in different genotypes. d Expression of PFL in different genotypes. Data in (c) and (d) are means ± SD (n = 5), and the P values were determined by a two-tailed unpaired Student’s t-test. Source data are provided as a Source Data file. e Model of ACL1–ROC4/5 complexes synergistically regulating drought tolerance and BPH resistance. When there are fewer ACL1 proteins, more ROC proteins are released to form homodimers or heterodimers. ROC4 regulates wax synthesis genes to promote wax synthesis, and ROC5 regulates BC-related genes to inhibit the overdevelopment of BC, thus promoting drought tolerance and increasing BPH resistance of the plants (left panel). Excessive ACL1 proteins could competitively bind with ROC4 and ROC5 to obstruct homodimer or heterodimer formation and recruit TOPLESS to form a complex to inhibit the downstream transcription of wax biosynthesis genes and BC-related genes, thus resulting in decreased wax content and an increase in the number and size of BCs, which promotes susceptibility to both drought and BPH (right panel).