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Title: RECESSIVE-INTERFERING MUTATIONS IN THE GIBBERELLIN SIGNALING GENE SLEEPY1 ARE RESCUED BY OVEREXPRESSION OF ITS HOMOLOGUE SNEEZY

Author
item STRADER, LUCIA - WASHINGTON STATE UNIV
item RITCHIE, SIAN - WASHINGTON STATE UNIV
item SOULE, JONATHAN - FORMER USDA-ARS
item MCGINNIS, KAREN - FORMER USDA-ARS
item Steber, Camille

Submitted to: Proceedings of the National Academy of Sciences (PNAS)
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/17/2004
Publication Date: 7/28/2004
Citation: Strader, L., Ritchie, S., Soule, J.D., Mcginnis, K.M., Steber, C.M. 2004. Recessive-interfering mutations in the ga-response gene sleepy1 are rescued by overexpression of its homologue sneezy. Proceedings of the National Academy of Sciences. 101:12771-12776.

Interpretive Summary: The plant hormone gibberellin (GA) controls important aspects of plant growth and development including germination, stem elongation, and transition to flowering. These processes are relevant to the agricultural traits of preharvest sprouting, emergence, lodging, earliness and yield. This paper reports the genetic interaction between two F-box genes, SLEEPY1 (SLY1) and SNEEZY (SNE), in the model plant Arabidopsis thaliana GA (gibberellin) signaling. The SLY1 gene encodes a positive regulator of GA signaling. The sly1-2 and sly1-10 mutants have recessive, GA-insensitive phenotypes including delayed germination, dwarfism, reduced fertility. The SLY1 gene is a negative regulator of the DELLA proteins, putative transcription factors that negatively regulate GA signaling. Mutations in the DELLA proteins resulted in the semidwarf varieties that drove the 20% increas in crop yield that is called the "green revoluation". This paper provides evidence that another Arabidopsis gene SNEEZY (SNE) that is similar to SLEEPY1 (SLY1) can freplace SLY1 by stimulating the disappearance of DELLA proteins. This hypothesis was supported because overexpression of SNE in sly1-10 mutants rescued the mutant's dwarfism.

Technical Abstract: This paper reports the genetic interaction of two F-box genes, SLEEPY1 (SLY1) and SNEEZY (SNE), in Arabidopsis thaliana GA (gibberellin) signaling. The SLY1 gene encodes an F-box subunit of an SCF E3 ubiquitin ligase complex that positively regulates GA signaling. The sly1-2 and sly1-10 mutants have recessive, GA-insensitive phenotypes including delayed germination, dwarfism, reduced fertility, and overaccumulation of the DELLA proteins RGA, GAI and RGL2. The DELLA proteins are putative transcription factors that negatively regulate GA signaling. The requirement for SLY1 in GA-stimulated disappearance of DELLA proteins suggests that GA targets DELLA proteins for destruction via SCFSLY1-mediated ubiquitylation. Overexpression of SLY1 in sly1-2 and sly1-10 plants rescues the recessive GA-insensitive phenotype of these mutants. Surprisingly, antisense expression of SLY1 also suppresses these mutants. This result caused us to hypothesize that the SLY1 homologue SNEEZY (SNE) can functionally replace SLY1 in the absence of the recessive interfering sly1-2 or sly1-10 genes. This hypothesis was supported because overexpression of SNE in sly1-10 rescues the dwarf phenotype. In addition to rescuing the sly1-10 dwarf phenotype, SNE overexpression also restored normal RGA protein levels, suggesting that the SNE F-box protein can replace SLY1 in the GA-induced proteolysis of RGA. If the C-terminal truncation in the sly1-2 and sly1-10 alleles interferes with SNE rescue, we reasoned that overexpression of sly1-2 might interfere with wild-type SLY1 function. Indeed, overexpression of sly1-2 in wild-type Ler (Landsberg erecta) yields dwarf plants.