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Title: Seed germination of GA-insensitive sleepy1 mutants does not require RGL2 protein disappearance in Arabidopsis

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

Submitted to: The Plant Cell
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/5/2007
Publication Date: 3/23/2007
Citation: Ariizumi, T., Steber, C.M. 2007. Seed germination of GA-insensitive sleepy1 mutants does not require RGL2 protein disappearance in Arabidopsis. The Plant Cell 19, 791-804.

Interpretive Summary: Seed germination is a complex developmental process regulated by phytohormones. The phytohormone abscisic acid (ABA) inhibits seed germination, whereas gibberellin (GA) stimulates seed germination. Recent evidence suggests GA stimulates seed germination by triggering destruction of DELLA family proteins. DELLA proteins are negative regulators of GA responses, and RGL2 is the main DELLA protein repressing seed germination. This study investigates one part of the seed germination puzzle.

Technical Abstract: 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. Preliminary experiments indicate that 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.