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SlMBD5 Promotes Seed Germination by Epigenetically Repressing the Gibberellin Catabolism Gene SlGA2ox4 in Tomato [RNA-Seq]

ABSTRACT: Seed germination represents a critical developmental transition in spermatophytes. Gibberellins (GAs) are essential phytohormones regulating seed germination. GA2-oxidases (GA2ox) play a key role in modulating GA levels by converting active GAs to inactive forms, critically influencing seed development and germination. How seed germination is epigenetically regulated by DNA methylation is poorly understood. Here, we identified the tomato methyl-CpG-binding domain (MBD) protein SlMBD5 as a regulator of seed germination. The slmbd5 mutant exhibits delayed germination and reduced GA4/GA7 levels, which can be rescued by exogenous GA4+7 application. Transcriptomic and biochemical analyses revealed that SlMBD5 represses the GA catabolism gene SlGA2ox4 by directly binding to its hypermethylated promoter. Furthermore, we show that SlMBD5 interacts with the histone methylation reader SlEBS, forming a functional complex that promotes the transcriptional repression of SlGA2ox4. Consistent with the model that SIMBD5 promotes seed germination through its repression of SlGA2ox4, the slmbd5/slga2ox4 double mutant shows partially restored germination. This study thus reveals an SlMBD5-SlEBS module that epigenetically regulates GA homeostasis to modulate seed germination in tomato.

ORGANISM(S): Solanum lycopersicum

PROVIDER: GSE285259 | GEO | 2025/12/22

REPOSITORIES: GEO

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SlMBD5 Promotes Seed Germination by Epigenetically Repressing the Gibberellin Catabolism Gene SlGA2ox4 in Tomato [ChIP-Seq]

Project description:Seed germination represents a critical developmental transition in spermatophytes. Gibberellins (GAs) are essential phytohormones regulating seed germination. GA2-oxidases (GA2ox) play a key role in modulating GA levels by converting active GAs to inactive forms, critically influencing seed development and germination. How seed germination is epigenetically regulated by DNA methylation is poorly understood. Here, we identified the tomato methyl-CpG-binding domain (MBD) protein SlMBD5 as a regulator of seed germination. The slmbd5 mutant exhibits delayed germination and reduced GA4/GA7 levels, which can be rescued by exogenous GA4+7 application. Transcriptomic and biochemical analyses revealed that SlMBD5 represses the GA catabolism gene SlGA2ox4 by directly binding to its hypermethylated promoter. Furthermore, we show that SlMBD5 interacts with the histone methylation reader SlEBS, forming a functional complex that promotes the transcriptional repression of SlGA2ox4. Consistent with the model that SIMBD5 promotes seed germination through its repression of SlGA2ox4, the slmbd5/slga2ox4 double mutant shows partially restored germination. This study thus reveals an SlMBD5-SlEBS module that epigenetically regulates GA homeostasis to modulate seed germination in tomato.

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Characterizing the expression, binding and function properties of Methyl-CpG-binding Domain (MBDs) genes in tomato [BS-Seq]

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The COP9 Signalosome regulates seed germination by facilitating protein degradation of RGL2 and ABI5

Project description:The control of seed germination and seed dormancy are critical for the successful propagation of plant species, and are important agricultural traits. Seed germination is tightly controlled by the balance of gibberellin (GA) and abscisic acid (ABA), and is influenced by environmental factors. The COP9 Signalosome (CSN) is a conserved multi-subunit protein complex that is best known as a regulator of the Cullin-RING family of ubiquitin E3 ligases (CRLs). Multiple viable mutants of the CSN showed poor germination, except for csn5b-1. Detailed analyses showed that csn1-10 has a stronger seed dormancy, while csn5a-1 mutants exhibit retarded seed germination in addition to hyperdormancy. Both csn5a-1 and csn1-10 plants show defects in the timely removal of the germination inhibitors: RGL2, a repressor of GA signaling, and ABI5, an effector of ABA responses. We provide genetic evidence to demonstrate that the germination phenotype of csn1-10 is caused by over-accumulation of RGL2, a substrate of the SCF (CRL1) ubiquitin E3 ligase, while the csn5a-1 phenotype is caused by over-accumulation of RGL2 as well as ABI5. The genetic data are consistent with the hypothesis that CSN5A regulates ABI5 by a mechanism that may not involve CSN1. Transcriptome analyses suggest that CSN1 has a more prominent role than CSN5A during seed maturation, but CSN5A plays a more important role than CSN1 during seed germination, further supporting the functional distinction of these two CSN genes. Our study delineates the molecular targets of the CSN complex in seed germination, and reveals that CSN5 has additional functions in regulating ABI5, thus the ABA signaling pathway.

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