Abstract

Seed dormancy controls germination and plays a critical role in regulating the beginning of the life cycle of plants. Seed dormancy is established and maintained during seed maturation and is gradually broken during dry storage (after-ripening). The plant hormone abscisic acid (ABA) and DELAY OF GERMINATION1 (DOG1) protein are essential regulators of seed dormancy. Recent studies revealed that chromatin modifications are also involved in the transcription regulation of seed dormancy. Here, we showed that two Arabidopsis histone demethylases, LYSINESPECIFIC DEMETHYLASE LIKE 1 and 2 (LDL1 and LDL2) act redundantly in repressing of seed dormancy. LDL1 and LDL2 are highly expressed in the early silique developing stage. The ldl1 ldl2 double mutant displays increased seed dormancy, whereas overexpression of LDL1 or LDL2 in Arabidopsis causes reduced dormancy. Furthermore, we showed that LDL1 and LDL2 repress the expression of seed dormancy-related genes, including DOG1, ABA2 and ABI3 during seed dormancy establishment. Furthermore, genetic analysis revealed that the repression of seed dormancy by LDL1 and LDL2 requires DOG1, ABA2, and ABI3. Taken together, our findings revealed that LDL1 and LDL2 play an essential role in seed dormancy.

Highlights

  • Accurate timing of seed germination requires a reliable control mechanism

  • Subcellular Localization of LDL1 and LDL2 To investigate the subcellular localization of LDL1 and LDL2 proteins, full-length coding sequences of LDL1 and LDL2 fused with yellow fluorescent protein (YFP) were delivered to the Arabidopsis protoplasts

  • LDL1 and LDL2 Repress DELAY OF GERMINATION1 (DOG1) Expression Previous work has demonstrated that DOG1 is the master regulator of seed dormancy which is only expressed in seed and its expression level increases during seed maturation (Bentsink et al, 2006)

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Summary

Introduction

Accurate timing of seed germination requires a reliable control mechanism. Seed dormancy is a major factor in this control, which refers to the seed property that incapacitates seed germination even under optimal conditions (Hilhorst, 2007). Seed dormancy prevents or delays the germination of maturated seed until conditions are favorable for starting a new life cycle. Seed dormancy is established during seed maturation, and dormancy has been shown to be imposed by the embryo, testa, endosperm or combinations of these tissues (Kim et al, 2013). Seed dormancy can be broken after a period of seed after-ripening or on seed stratification, that is, exposure to cold and moist conditions.

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