Figure 11.

Model of how OsDET1 deficiency leads to contradictory phenotypes related to ABA in OsDET1 RNAi plants. OsDDB1 interacts with OsCOP10, OsDET1, and OsDDA1 to form the CDDD complex. The reduction of CDDD complex function hinders the ubiquitination of OsPYLs and causes the accumulation of OsPYLs. The accumulation of PYLs and ABA promotes the stability of the PP2C-ABA-PYL ternary complex (Irigoyen et al., 2014). However, OsDET1 deficiency also leads to a decline in the content of ABA in normal conditions. Thus, due to these opposing factors, OsDET1 deficiency only partly causes the ABA hypersensitivity phenotype, such as closed stomatal pores and changes of pollen grain morphology, although it is unable to induce leaf senescence in normal development. The modulation of cuticular wax biosynthesis by the ABA signaling pathway is distinct from the governing stomatal regulation, and the accumulation of cuticular waxes is reduced in OsDET1 RNAi plants. During dark treatment, ABA is induced by continuous dark, which further enhances the ABA response and finally leads to increased leaf senescence. The leaf senescence in turn promotes the synthesis of ABA. Finally, OsDET1 RNAi plants exhibit a significantly accelerated leaf senescence phenotype.