ARS | Publication request: Proteolysis-independent down-regulation of DELLA repression by the gibberellin receptor GID1

Submitted to: The Plant Cell
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 1, 2008
Publication Date: September 30, 2008
Citation: Ariizumi, T., Murase, K., Sun, T.P., Steber, C.M. 2008. Proteolysis-independent down-regulation of DELLA repression by the gibberellin receptor GID1. The Plant Cell.

Interpretive Summary: This paper examines the genes and proteins that control the decision to germinate, stem elongation, and plant fertility. The DELLA genes are negative regulators of germination, stem elongation and flowering. DELLAs are important to agriculture in part because they are the green revolution genes (RHT in wheat) and because the govern important traits such as preharvest sprouting, seedling emergence, lodging tolerance, and yield. Previous work suggests that the growth hormone GA stimulates all of these developmental events by causing the destruction of DELLA. However, there are situations in which DELLA cannot be destroyed such as under disease of environmental stress. This work shows that DELLA repression can also be switched off in the absence of DELLA destruction. This result transforms the model for the control of crop plant development and may provide new tools for controlling important agricultural traits.

Technical Abstract: This paper presents evidence for proteolysis-independent regulation of DELLA repression of gibberellin (GA) signaling in Arabidopsis. DELLA proteins are negative regulators of GA responses including seed germination, stem elongation, and fertility. GA can stimulate GA responses by causing proteolysis of DELLA repressors by the ubiquitin-proteasome pathway. This destruction requires GA biosynthesis, three functionally redundant GA receptors GIBBERELLIN INSENSITIVE DWARF1 (GID1a, GID1b and GID1c), and the SLEEPY1 (SLY1) F-box subunit of an SCF E3 ubiquitin ligase. Using sly1 mutants in which DELLA proteins remain stable after GA application, we found that GA regulates DELLA repressor activity by a mechanism distinct from protein destruction. Overexpression of GID1 genes rescued the dwarf and infertility phenotypes of the sly1 mutants without altering accumulation of DELLA proteins RGA and GAI. This rescue required GA biosynthesis and the presence of a functional DELLA motif in RGA and GAI. Both the DELLA motif and GA are required for the protein interaction of DELLA protein and GID1. The sly1 mutants display a less severe dwarf phenotype than the GA biosynthesis mutant ga1-3 or the gid1a gid1b gid1c triple mutant despite the fact that sly1 mutants accumulate far higher levels of DELLA protein. Based on double mutant analysis, it appears that both intermediate phenotype and high level DELLA accumulation in sly1 mutants require GA and a functional DELLA motif. These results suggest that GA-bound GID1 can block DELLA repressor activity by direct protein-protein interaction with the DELLA domain, and that this interaction may lead to increased DELLA accumulation.