Dataset Information

PsRGL1 negatively regulates chilling- and gibberellin-induced dormancy release by PsF-box1-mediated targeting for proteolytic degradation in tree peony.

ABSTRACT: Tree peony bud endodormancy is a common survival strategy similar to many perennial woody plants in winter, and the activation of the GA signaling pathway is the key to breaking endodormancy. GA signal transduction is involved in many physiological processes. Although the GA-GID1-DELLA regulatory module is conserved in many plants, it has a set of specific components that add complexity to the GA response mechanism. DELLA proteins are key switches in GA signaling. Therefore, there is an urgent need to identify the key DELLA proteins involved in tree peony bud dormancy release. In this study, the prolonged chilling increased the content of endogenously active gibberellins. PsRGL1 among three DELLA proteins was significantly downregulated during chilling- and exogenous GA₃-induced bud dormancy release by cell-free degradation assay, and a high level of polyubiquitination was detected. Silencing PsRGL1 accelerated bud dormancy release by increasing the expression of the genes associated with dormancy release, including PsCYCD, PsEBB1, PsEBB3, PsBG6, and PsBG9. Three F-box protein family members responded to chilling and GA₃ treatments, resulting in PsF-box1 induction. Yeast two-hybrid and BiFC assays indicated that only PsF-box1 could bind to PsRGL1, and the binding site was in the C-terminal domain. PsF-box1 overexpression promoted dormancy release and upregulated the expression of the dormancy-related genes. In addition, yeast two-hybrid and pull-down assays showed that PsF-box1 also interacted with PsSKP1 to form an E3 ubiquitin ligase. These findings enriched the molecular mechanism of the GA signaling pathway during dormancy release, and enhanced the understanding of tree peony bud endodormancy.

SUBMITTER: Gao L

PROVIDER: S-EPMC10541556 | biostudies-literature | 2023 May

REPOSITORIES: biostudies-literature

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PsRGL1 negatively regulates chilling- and gibberellin-induced dormancy release by PsF-box1-mediated targeting for proteolytic degradation in tree peony.

Gao Linqiang L Niu Demei D Chi Tianyu T Yuan Yanchao Y Liu Chunying C Gai Shupeng S Zhang Yuxi Y

Horticulture research 20230313 5

Tree peony bud endodormancy is a common survival strategy similar to many perennial woody plants in winter, and the activation of the GA signaling pathway is the key to breaking endodormancy. GA signal transduction is involved in many physiological processes. Although the GA-GID1-DELLA regulatory module is conserved in many plants, it has a set of specific components that add complexity to the GA response mechanism. DELLA proteins are key switches in GA signaling. Therefore, there is an urgent n ...[more]

PMID: 37786434

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Project description:BackgroundThe complete dormancy release determines the quality of bud break, flowering and fruiting. While in tree peony (Paeonia suffruticosa Andr.), the insufficient accumulation of cold temperatures results in incomplete dormancy release and poor flowering quality.ResultsIn order to investigate if phytohormone can replace the chilling requirement in south China and other similar regions, the roles of fluridone (Flu), gibberellin (GA3), and their combination in the bud dormancy release process were analyzed. It demonstrated that the application of exogenous GA3 and the mixture significantly expedited the dormancy release of tree peony at 23℃. Furthermore, the endogenous hormone levels provided evidence for the substantial impact of exogenous GA3 on dormancy release, highlighting its potential involvement in the chilling-independent pathway of dormancy release. Transcriptome sequencing and analysis of expression profiles were conducted to identify the crucial genes implicated in the dormancy release mechanism of tree peony. Among numerous genes from diverse gene families, the particularly interesting were TEOSINTE BRANCHED 1, CYCLOIDEA, and PROLIFERATING CELL FACTORS-like genes (PsTCP3, PsTCP4, and PsTCP14), which had significant expression levels during the dormancy release process under different treatments. They were divided into two distinct sub-families based on their different domains. Specifically, PsTCP14 was classified under Class I, while PsTCP3 and PsTCP4 were classified under Class II. The analysis of expression patterns revealed a significant accumulation of the three PsTCPs in buds undergoing dormancy release, with clear upregulation observed in response to GA3 and the mixture treatments. Additionally, the analysis of promoter activity demonstrated the sensitivity of PsTCP4 and PsTCP14 to GA3 and Flu.ConclusionThe application of exogenous GA3 has been shown to effectively expedite the release of dormancy in tree peony through a pathway that is not dependent on chilling. Further research found that PsTCP genes might play a crucial role in this process. These findings contribute to the understanding of the molecular mechanism of PsTCPs in the hormone-mediated and temperature-independent release of bud dormancy in tree peony.

Project description:Background and aimsThe tree peony (Paeonia suffruticosa Andr.) has been widely cultivated as a field plant, and petal blotch is one of its important traits, which not only promotes proliferation but also confers high ornamental value. However, the regulatory network controlling blotch formation remains elusive owing to the functional differences and limited conservation of transcriptional regulators in dicots.MethodsWe performed phylogenetic analysis to identify MYB44-like transcription factors in P. suffruticosa blotched cultivar 'High noon' petals. A candidate MYB44-like transcription factor, PsMYB44, was analysed via expression pattern analysis, subcellular localization, target gene identification, gene silencing in P. suffruticosa petals and heterologous overexpression in tobacco.Key resultsA blotch formation-related MYB44-like transcription factor, PsMYB44, was cloned. The C-terminal of the PsMYB44 amino acid sequence had a complete C2 motif that affects anthocyanin biosynthesis, and PsMYB44 was clustered in the MYB44-like transcriptional repressor branch. PsMYB44 was located in the nucleus, and its spatial and temporal expression patterns were negatively correlated with blotch formation. Furthermore, a yeast one-hybrid assay showed that PsMYB44 could target the promoter of the late anthocyanin biosynthesis-related dihydroflavonol-4-reductase (DFR) gene, and a dual-luciferase assay demonstrated that PsMYB44 could repress PsDFR promoter activity. On the one hand, overexpression of PsMYB44 significantly faded the red colour of tobacco flowers and decreased the anthocyanin content by 42.3 % by downregulating the expression level of the tobacco NtDFR gene. On the other hand, PsMYB44-silenced P. suffruticosa petals had a redder blotch colour, which was attributed to the fact that silencing PsMYB44 redirected metabolic flux to the anthocyanin biosynthesis branch, thereby promoting more anthocyanin accumulation in the petal base.ConclusionThese results demonstrated that PsMYB44 negatively regulated the biosynthesis of anthocyanin by directly binding to the PsDFR promoter and subsequently inhibiting blotch formation, which helped to elucidate the molecular regulatory network of anthocyanin-mediated blotch formation in plants.

Dataset Information

PsRGL1 negatively regulates chilling- and gibberellin-induced dormancy release by PsF-box1-mediated targeting for proteolytic degradation in tree peony.

Publications

PsRGL1 negatively regulates chilling- and gibberellin-induced dormancy release by PsF-box1-mediated targeting for proteolytic degradation in tree peony.

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