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Title: Loss of Arabidopsis thaliana seed dormancy is associated with increased accumulation of the GID1 GA hormone receptors

item HAUVERMALE, AMBER - Washington State University
item TUTTLE, KEIKO - Washington State University
item TAKEBAYASHI, YUMIKO - Riken Institute
item MITSUNORI, SEO - Riken Institute
item Steber, Camille

Submitted to: Plant Cell Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/1/2015
Publication Date: 9/8/2015
Citation: Hauvermale, A.L., Tuttle, K.M., Takebayashi, Y., Mitsunori, S., Steber, C.M. 2015. Loss of Arabidopsis thaliana seed dormancy is associated with increased accumulation of the GID1 GA hormone receptors. Plant Cell Physiology. 56(9):1773-1785.

Interpretive Summary: The control of seed germination is essential in all crops plants. Even seed germination and seedling emergence is essential to obtaining good stand establishment and yield. And in cereals, seed dormancy is essential to preventing preharvest sprouting if rain occurs before harvest. This study places an important puzzle piece into the seed dormancy/germination jigsaw puzzle, by showing that loss of seed dormancy prepares a seed/plant embryo to respond to the germination hormone GA. The receptor protein that hears the GA signal, GID1 (GA-insensitive dwarf), is activated in response to dormancy loss through dry storage/after-ripening and through moist chilling. This tells us that the GA receptor is likely a good marker to judge the ability of a seed to germinate.

Technical Abstract: Two hormone signaling pathways regulate the transition from seed dormancy to germination; abscisic acid (ABA) establishes and maintains seed dormancy and gibberellin (GA) stimulates seed germination. Seed dormancy prevents the germination of young seeds, providing time for seed dispersal and ensuring germination in the appropriate season and condition. Seed dormancy is lost through a period of dry storage called after-ripening or through moist chilling (cold stratification). Both of these treatments are associated with decreased ABA accumulation, but increased GA hormone levels have been detected only with cold stratification. After-ripening and cold stratification act additively to enhance GA hormone sensitivity in ga1-3 seeds that cannot synthesize GA. The effect of these dormancy-breaking treatments is enhanced by overexpression of the GA receptor genes, GID1a, GID1b, GID1c (GA-INSENSITIVE DWARF), but GID1b has the strongest effect. After-ripening induces GID1b, but not GID1a or GID1c mRNA accumulation. The rise in GID1b transcript with after-ripening was not associated with decreases in ABA levels, suggesting that GID1 regulation by after-ripening is ABA-independent. Cold stratification stimulated the accumulation of all three GID1 transcripts. However, cold stratification resulted in no increase in GA sensitivity during ga1-3 seed germination unless seeds were after-ripened. This may be due to the fact that after-ripening stimulates HA:GID1a, HA:GID1b, and HA:GID1c protein accumulation independently of transcript abundance. The three GID1 GA receptor transcripts showed other differences in expression pattern. GID1b transcript accumulation depended most strongly on DELLA RGL2, whereas GID1a and GID1c were more strongly down-regulated in the dark.