ABA is a stress responsive phytohormone which inhibits seed germination and seedling growth to adapt to unfavorable environmental conditions while GA is a major growth promoting phytohormone which promotes seed germination, seedling growth, flowering and leaf expansion. Recent studies have portrayed a conceptual ABA signaling pathway in which ABA binds to its receptor PYL/PYR/RCARs, subsequently the PYL/PYR/RCAR-ABA complex binds to PP2C phosphatases which repress the SnRK2s, releasing the activated SnRK2s to phosphorylate downstream targets to activate ABA responses. In the GA signaling pathway, the receptor GID1 and E3 ligase SCFSLY1/GID2 together promote the degradation of the DELLA repressor proteins in a GA-dependent manner to relieve their repression of GA action. Although recent studies have shown that ABA can antagonize GA-promoted degradation of DELLA proteins, the regulatory mechanism underlying the antagonism of GA on ABA signaling pathway remains largely unknown.

Recently, the Innovation Team of Crop Functional Genomics from Institute of Crop Science (ICS) of Chinese Academy of Agricultural Sciences (CAAS) has made a progress in decoding the antagonism mechanism of GA on ABA signaling pathway.

In a previous study, they reported that rice Tiller Enhancer (TE) encodes an activator of the APC/CTE E3 ubiquitin ligase complex that acts to repress tillering (branching) by promoting the degradation of MOC1, a master regulator of plant architecture and tiller number. In addition to increased tillers, the te mutant also displays reduced height, twisted flag leaf and panicles, suggesting that TE regulates other developmental processes.