RGL2 PROTEIN DOES NOT DISAPPEAR DURING SLY1 MUTANT SEED GERMINATION

Authors: ARIIZUMI, TOHRU - WASHINGTON STATE UNIV; Steber, Camille

Submitted to: International Conference on Plant Growth Substances Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 4/1/2007
Publication Date: 7/1/2007
Citation: Ariizumi, T., Steber, C.M. 2007. Rgl2 protein does not disappear during sly1 mutant seed germination. International Conference on Plant Growth Substances Proceedings, July 21-25, Puerta Vallerta, Mexico, MS705.

Interpretive Summary:

Technical Abstract: The SLEEPY1 (SLY1) and RGA-like2 (RGL2) genes play an important role in the regulation of seed germination by GA in Arabidopsis. The control of seed dormancy and germination is critical for plant survival and important for proper stand establishment in crop species. The plant hormone gibberellin (GA) stimulates seed germination in many plant species and is required for seed germination in Arabidopsis. The Arabidopsis GA biosynthesis mutant ga1-3 is unable to germinate unless GA is exogenously applied. The failure of seed germination in ga1-3 is suppressed by mutations in RGL2, and GA stimulation of germination in ga1-3 is associated with rapid disappearance of RGL2 protein. This suggests that the RGL2 DELLA protein is an important repressor of seed germination. The current model is that GA stimulates seed germination by causing the SLY1 SCF complex to trigger the ubiquitination and destruction of the RGL2 protein. Unlike ga1-3, the GA-insensitive sly1 mutant shows a variable seed dormancy phenotype. Those seed lots showing high seed dormancy eventually afterripen. Stronger alleles showed a stronger seed germination phenotype and required more time to afterripen. It was expected that if RGL2 is the major repressor of seed germination, sly1 mutant seeds that germinate well should accumulate lower levels of RGL2 protein than those that fail to germinate. Surprisingly, RGL2 protein accumulated at high levels even in after-ripened sly1 mutant seeds capable of 100% seed germination. RGL2 protein accumulation actually appeared to be higher in sly1-10 which shows a milder seed germination phenotype than the sly1-2 allele. This suggests that SCFSLY1 is the main E3 ubiquitin ligase controlling RGL2 protein accumulation, and that RGL2 disappearance is not a prerequisite for seed germination in the sly1 mutant background. In the absence of GA, several GA-induced genes show increased accumulation in sly1 mutant seeds compared to ga1-3. It is possible, that the RGL2 repressor of seed germination is inactivated by after-ripening of sly1 mutant seeds or that a parallel pathway controls seed dormancy and germination in the sly1 mutant background.