Fig. 7

A hypothetical model illustrating the RAE1-STOP1 module in regulation of ABA sensitivity in Arabidopsis early seedlings. Exogenous ABA treatment induces the expression of Arabidopsis RAE1, which facilitates the ubiquitination and degradation of STOP1 in wild-type plants. In the rae1 mutant, the absence of RAE1-mediated degradation leads to STOP1 accumulation, resulting in enhanced ABA perception and signaling characterized by ABI5 upregulation. This increase in ABI5 stimulates the expression of target genes such as MFT, EM6, RAB18, and RD29B, contributing to heightened ABA sensitivity in early seedlings. Therefore, the RAE1-STOP1 module functions as a regulatory mechanism to reduce ABA sensitivity by inhibiting ABI5 elevation during the early seedling stage in Arabidopsis. In the STOP1 dysfunctional alleles, a still unknown mediator/complimentary pathway enhances ABA perception and signaling, resulting in the activation of ABA-responsive genes (excluding MFT) and an increased ABA response. Notably, reduced ABI5 levels and the lack of MFT expression changes in the STOP1 dysfunctional allele distinguish it from the rae1 and STOP1OE lines. This reveals a possible bidirectional modulation of ABA sensitivity by STOP1 protein levels during the early seedling stage. Disrupted STOP1 protein homeostasis in both STOP1 upregulation lines (i.e., rae1 mutant and STOP1 overexpression lines) and STOP1 dysfunctional alleles confers increased ABA sensitivity