AI Article Synopsis
- The phytohormones abscisic acid (ABA) and gibberellic acid (GA) work against each other to control seed dormancy and germination.
- DELAY OF GERMINATION1 (DOG1) is a key regulator involved in seed dormancy, but its regulatory mechanisms are not fully understood.
- This study identifies a module involving the bHLH transcriptional factor WRKY36 and its interactions with AFP2 and TPR2 that epigenetically represses DOG1, thereby regulating seed dormancy and promoting germination.
Article Abstract
The phytohormones abscisic acid (ABA) and gibberellic acid (GA) antagonistically control the shift between seed dormancy and its alleviation. DELAY OF GERMINATION1 (DOG1) is a critical regulator that determines the intensity of primary seed dormancy, but its underlying regulatory mechanism is unclear. In this study, we combined physiological, biochemical, and genetic approaches to reveal that a bHLH transcriptional factor WRKY36 progressively silenced DOG1 expression to break seed dormancy through ABI5-BINDING PROTEIN 2 (AFP2) as the negative regulator of ABA signal. AFP2 interacted with WRKY36, which recognizes the W-BOX in the DOG1 promoter to suppress its expression; Overexpressing WRKY36 broke primary seed dormancy, whereas wrky36 mutants showed strong primary seed dormancy. In addition, AFP2 recruited the transcriptional corepressor TOPLESS-RELATED PROTEIN2 (TPR2) to reduce histone acetylation at the DOG1 locus, ultimately mediating WRKY36-dependent inhibition of DOG1 expression to break primary seed dormancy. Our result proposes that the WRKY36-AFP2-TPR2 module progressively silences DOG1 expression epigenetically, thereby fine-tuning primary seed dormancy.
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| http://dx.doi.org/10.1111/nph.18750 | DOI Listing |
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