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Title: The role of the GA signaling SLY1 in Arabidopsis seed germination

item Steber, Camille

Submitted to: Seed Biology: Advances and Applications
Publication Type: Abstract Only
Publication Acceptance Date: 10/1/2006
Publication Date: 12/1/2006
Citation: Steber, C.M. 2006. The role of the GA signaling SLY1 in Arabidopsis seed germination. Seed Biology: Advances and Applications. W1168 Seed Biology Group, San Antonio, TX, Dec 1-4, pg. 127.

Interpretive Summary:

Technical Abstract: Seed dormancy, afterripening, and germination are complex developmental process regulated by phytohormones. The phytohormone abscisic acid (ABA) is needed to set up seed dormancy during embryo maturation whereas gibberellin (GA) stimulates seed germination. In tomato and Arabidopsis, GA is clearly required for seed germination. Recent evidence suggests that GA stimulates seed germination by triggering destruction of DELLA family proteins via the SCF-SLY1 E3 ubiquitin ligase and the 26S proteosome pathway. DELLA proteins are negative regulators of GA responses, and RGL2 is the main DELLA protein repressing seed germination. SLY1 appears to tranduce the GA signal by triggering DELLA destruction by ubiquitination. GA-insensitive sly1 mutants resemble GA biosynthesis mutants in that they exhibit dwarfism, late flowering, reduced fertility and increased seed dormancy. These sly1 phenotypes are not rescued by GA application and are not as severe as those seen in the ga1-3 GA biosynthesis mutant. While the ga1-3 mutant fails to germinate in the absence of GA, the seed germination rate varies greatly (3-100%) among independent seed lots of young sly1 mutants. Dormant sly1 seeds eventually afterripen. However even sly1 mutant seeds that can germinate do so more slowly than WT and show greater sensitivity to ABA and reduced osmotic potential. The germination of dormant sly1 mutant seed lots improved following afterripening. To better understand the sly1 mutant seed germination phenotype, we examined the effect of these mutations on RGL2 protein accumulation. It is known that high levels of RGL2 protein in the ga1-3 mutant correlates with failure to germinate, and that mutations in RGL2 suppress the ga1-3 seed germination phenotype. sly1 mutants are able to germinate even when high levels of RGL2 protein are present. This suggests that protein disappearance may not be the only mechanism controlling RGL2 activity.