Abstract
Summary DELAY OF GERMINATION1 (DOG1) is a primary regulator of seed dormancy. Accumulation of DOG1 in seeds leads to deep dormancy and delayed germination in Arabidopsis. B3 domain‐containing transcriptional repressors HSI2/VAL1 and HSL1/VAL2 silence seed dormancy and enable the subsequent germination and seedling growth. However, the roles of HSI2 and HSL1 in regulation of DOG1 expression and seed dormancy remain elusive.Seed dormancy was analysed by measurement of maximum germination percentage of freshly harvested Arabidopsis seeds. In vivo protein–protein interaction analysis, ChIP‐qPCR and EMSA were performed and suggested that HSI2 and HSL1 can form dimers to directly regulate DOG1.HSI2 and HSL1 dimers interact with RY elements at DOG1 promoter. Both B3 and PHD‐like domains are required for enrichment of HSI2 and HSL1 at the DOG1 promoter. HSI2 and HSL1 recruit components of polycomb‐group proteins, including CURLY LEAF (CLF) and LIKE HETERCHROMATIN PROTEIN 1 (LHP1), for consequent deposition of H3K27me3 marks, leading to repression of DOG1 expression.Our findings suggest that HSI2‐ and HSL1‐dependent histone methylation plays critical roles in regulation of seed dormancy during seed germination and early seedling growth.
Highlights
Seed dormancy is an adaptive mechanism that allows for the dispersal and survival of seeds over distance and time, and ensures that germination occurs under favorable conditions (Finch-Savage et al, 2006)
Analysis of the rates of germination of freshly-harvested seeds from these Arabidopsis lines confirmed that loss-of-function mutations in both hsi2 and hsl1 are necessary for significant increases in seed dormancy to be detected (Figure 1B)
The gain-offunction mutant dog1-5, which shows strongly delayed germination, and the loss-of-function mutant dog1-3, which shows early germination, served as controls in this assay. These results indicate that HIGH-LEVEL EXPRESSION OF SUGAR INDUCIBLE2 (HSI2) and HSL1 act redundantly to repress DELAY OF GERMINATION1 (DOG1) expression in seeds
Summary
Seed dormancy is an adaptive mechanism that allows for the dispersal and survival of seeds over distance and time, and ensures that germination occurs under favorable conditions (Finch-Savage et al, 2006). Seed dormancy is a complex trait that is regulated by both phytohormones and genetic factors. Abscisic acid (ABA) plays an important role in initiating and enhancing seed dormancy, while the dormant state is reversed by gibberellins, which promote germination under favorable conditions (Koornneef et al, 2002; Liu et al, 2010). GERMINATION1 (DOG1) was reported to be a major quantitative trait locus for the genetic regulation of seed dormancy in Arabidopsis (Alonso-Blanco et al, 2003; Bentsink et al, 2006, 2010; Huang et al, 2010). DOG1 acts in parallel with ABA to delay germination (Graeber et al, 2014) and, since DOG1 requires the clade A PP2C phosphatases
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