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Title: THE ROLE OF THE SLEEPY1 (SLY1) F-BOX GENE IN GA REGULATION OF SEED GERMINATION IN ARABIDOPSIS

Author
item ARIIZUMI, TOHRU - WASHINGTON STATE UNIV
item SCHRAMM, ELIZABETH - WASHINGTON STATE UNIV
item Steber, Camille

Submitted to: Arabidopsis Research International Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 4/18/2006
Publication Date: 6/15/2006
Citation: Ariizumi, T., Schramm, E., Steber, C.M. 2006. The role of the sleepy1 (sly1) f-box gene in ga regulation of seed germination in arabidopsis. Arabidopsis Res Intern Conference Proceedings. June 28-July 2, Madison, WI. Abst #378.

Interpretive Summary:

Technical Abstract: 17th International Conference on Arabidopsis Research, June 28-July 2, 2006, Madison, WI. Abstract #378. Seed germination is a complex developmental process regulated by phytohormones. The phytohormone abscisic acid (ABA) inhibits seed germination, 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 SCFSLY1 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. When sly1 mutant seeds can germination, they germinate 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. Consistent with the notion that SLY1 regulates seed germination, a SLY1 promoter::GUS fusion shows expression in the radicle during seed germination. To better understand the sly1 mutant seed germination phenotype, we are examining 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.