Bud Endodormancy Research Articles

Physiological and transcriptomic characterization of cold acclimation in endodormant grapevine under different temperature regimes.

It is essential for the survival of grapevines in cool climate viticultural regions where vines properly acclimate in late fall and early winter and develop freezing tolerance. Climate change-associated abnormities in temperature during the dormant season, including oscillations between prolonged warmth in late fall and extreme cold in midwinter, impact cold acclimation and threaten the sustainability of the grape and wine industry. We conducted two experiments in controlled environment to investigate the impacts of different temperature regimes on cold acclimation ability in endodormant grapevine buds through a combination of freezing tolerance-based physiological and RNA-seq-based transcriptomic monitoring. Results show that exposure to a constant temperature, whether warm (22 and 11°C), moderate (7°C), or cool (4 and 2°C) was insufficient for triggering cold acclimation and increasing freezing tolerance in dormant buds. However, when the same buds were exposed to temperature cycling (7±5°C), acclimation occurred, and freezing tolerance was increased by 5°C. We characterized the transcriptomic response of endodormant buds to high and low temperatures and temperature cycling and identified new potential roles for the ethylene pathway, starch and sugar metabolism, phenylpropanoid regulation, and protein metabolism in the genetic control of endodormancy maintenance. Despite clear evidence of temperature-responsive transcription in endodormant buds, our current understanding of the genetic control of cold acclimation remains a challenge when generalizing across grapevine tissues and phenological stages.

Deciphering the genetic mechanisms of chilling requirement for bud endodormancy release in deciduous fruit trees.

Bud endodormancy in deciduous fruit trees is an adaptive trait evolved by selection for the capacity to survive unfavorable environmental conditions. Deciduous trees require a certain amount of winter chill named chilling requirement (CR) to promote bud endodormancy release. In recent decades, global warming has endangered the chill accumulation in deciduous fruit trees. Developing low-CR cultivars is a practical way to neutralize the effect of climate changes on the cultivation and distribution of deciduous fruit trees. In this review, we focus on the effect of chilling accumulation on bud endodormancy release and the genetic mechanisms underlying the chilling requirement in deciduous fruit trees. Additionally, we put forth a regulatory model for bud endodormancy and provide prospective directions for future research in deciduous fruit trees.

PsSOC1 is involved in the gibberellin pathway to trigger cell proliferation and budburst during endodormancy release in tree peony.

Tree peony (Paeonia suffruticosa) undergoes bud endodormancy, and gibberellin (GA) pathway plays a crucial role in dormancy regulation. Recently, a key DELLA protein PsRGL1 has been identified as a negative regulator of bud dormancy release. However, the mechanism of GA signal to break bud dormancy remains unknown. In this study, yeast two-hybrid screened PsSOC1 interacting with PsRGL1 through its MADS domain, and interaction was identified using pull-down and luciferase complementation imaging assays Transformation in tree peony and hybrid poplar confirmed that PsSOC1 facilitated bud dormancy release. Transcriptome analysis of PsSOC1-overexpressed buds indicated PsCYCD3.3 and PsEBB3 were its potential downstream targets combining with promoter survey, and they also accelerated bud dormancy release verified by genetic analysis. Yeast one-hybrid, electrophoretic mobility shifts assays, chromatin immunoprecipitation quantitative PCR, and dual luciferase assays confirmed that PsSOC1 could directly bind to the CArG motif of PsCYCD3.3 and PsEBB3 promoters via its MADS domain. PsRGL1-PsSOC1 interaction inhibited the DNA-binding activity of PsSOC1. Additionally, PsCYCD3.3 promoted bud dormancy release by rebooting cell proliferation. These findings elucidated a novel GA pathway, GA-PsRGL1-PsSOC1-PsCYCDs, which expanded our understanding of the GA pathway in bud dormancy release.

Similar chilling response of dormant buds in potato tuber and woody perennials.

Bud dormancy is a survival strategy that plants have developed in their native habitats. It helps them endure harsh seasonal changes by temporarily halting growth and activity until conditions become more favorable. Research has primarily focused on bud dormancy in tree species and the ability to halt growth in vegetative tissues, particularly in meristems. Various plant species, such as potato, have developed specialized storage organs, enabling them to become dormant during their yearly growth cycle. Deciduous trees and potato tubers exhibit a similar type of bud endodormancy, where the bud meristem will not initiate growth, even under favorable environmental conditions. Chilling accumulation activates C-repeat/dehydration responsive element binding (DREB) factors (CBFs) transcription factors that modify the expression of dormancy-associated genes. Chilling conditions shorten the duration of endodormancy by influencing plant hormones and sugar metabolism, which affect the timing and rate of bud growth. Sugar metabolism and signaling pathways can interact with abscisic acid, affecting the symplastic connection of dormant buds. This review explores how chilling affects endodormancy duration and explores the similarity of the chilling response of dormant buds in potato tubers and woody perennials.

Establishment of a Homologous Silencing System with Intact-Plant Infiltration and Minimized Operation for Studying Gene Function in Herbaceous Peonies.

Gene function verification is a crucial step in studying the molecular mechanisms regulating various plant life activities. However, a stable and efficient homologous genetic transgenic system for herbaceous peonies has not been established. In this study, using virus-induced gene silencing technology (VIGS), a highly efficient homologous transient verification system with distinctive advantages was proposed, which not only achieves true "intact-plant" infiltration but also minimizes the operation. One-year-old roots of the representative species, Paeonia lactiflora Pall., were used as the materials; prechilling (4 °C) treatment for 3-5 weeks was applied as a critical precondition for P. lactiflora to acquire a certain chilling accumulation. A dormancy-related gene named HOMEOBOX PROTEIN 31 (PlHB31), believed to negatively regulate bud endodormancy release (BER), was chosen as the target gene in this study. GFP fluorescence was detected in directly infiltrated and newly developed roots and buds; the transgenic plantlets exhibited remarkably earlier budbreak, and PlHB31 was significantly downregulated in silenced plantlets. This study established a homologous transient silencing system featuring intact-plant infiltration and minimized manipulation for gene function research, and also offers technical support and serves as a theoretical basis for gene function discovery in numerous other geophytes.

Characterization of the MIKCC-type MADS-box gene family in blueberry and its possible mechanism for regulating flowering in response to the chilling requirement.

The expression peak of VcAP1.4, VcAP1.6, VcAP3.1, VcAP3.2, VcAG3, VcFLC2, and VcSVP9 coincided with the endo-dormancy release of flower buds. Additionally, GA4+7 not only increased the expression of these genes but also promoted flower bud endo-dormancy release. The MIKCC-type MADS-box gene family is involved in the regulation of flower development. A total of 109 members of the MIKCC-type MADS-box gene family were identified in blueberry. According to the phylogenetic tree, these 109 MIKCC-type MADS-box proteins were divided into 13 subfamilies, which were distributed across 40 Scaffolds. The results of the conserved motif analysis showed that among 20 motifs, motifs 1, 3, and 9 formed the MADS-box structural domain, while motifs 2, 4, and 6 formed the K-box structural domain. The presence of 66 pairs of fragment duplication events in blueberry suggested that gene duplication events contributed to gene expansion and functional differentiation. Additionally, the presence of cis-acting elements revealed that VcFLC2, VcAG3, and VcSVP9 might have significant roles in the endo-dormancy release of flower buds. Meanwhile, under chilling conditions, VcAP3.1 and VcAG7 might facilitate flower bud dormancy release. VcSEP11 might promote flowering following the release of endo-dormancy, while the elevated expression of VcAP1.7 (DAM) could impede the endo-dormancy release of flower buds. The effect of gibberellin (GA4+7) treatment on the expression pattern of MIKCC-type MADS-box genes revealed that VcAP1.4, VcAP1.6, VcAP3.1, VcAG3, and VcFLC2 might promote flower bud endo-dormancy release, while VcAP3.2, VcSEP11, and VcSVP9 might inhibit its endo-dormancy release. These results indicated that VcAP1.4, VcAP1.6, VcAP1.7 (DAM), VcAP3.1, VcAG3, VcAG7, VcFLC2, and VcSVP9 could be selected as key regulatory promoting genes for controlling the endo-dormancy of blueberry flower buds.

Screening and Expression Analysis of POD Gene in POD-H2O2 Pathway on Bud Dormancy of Pear (Pyrus pyrifolia)

Bud endodormancy represents a pivotal and intricate biological process influenced by both genetic and epigenetic factors, the exact mechanism of which remains elusive. Hydrogen peroxide (H2O2) functions as a signalling molecule in the regulation of dormancy, with peroxidase (POD) playing a crucial role in governing H2O2 levels. Our prior transcriptomic and metabolomic investigations into diverse pear dormancy phases posited that POD predominantly oversees pear bud dormancy. In this study, we utilised qRT-PCR to screen the most significantly expressed gene, Pyrus pyrifolia POD4-like (PpPOD4-like), from seven POD genes. Subsequently, H2O2 test kits, overexpression methods, and subcellular localisation techniques were employed to assess changes in H2O2 content, POD activity, PpPOD4-like expression, and its cellular positioning during pear bud dormancy. Subcellular localisation experiments revealed that PpPOD4-like is situated on the cell membranes. Notably, H2O2 content exhibited a rapid increase during endodormancy and decreased swiftly after ecodormancy. The fluctuation pattern of POD activity aligned with that of H2O2 content. Additionally, PpPOD4-like expression was markedly upregulated, displaying an overall upward trajectory. Our findings indicate that PpPOD4-like modulates H2O2 levels by regulating POD activity, thereby actively participating in the intricate regulation of pear dormancy processes.

PsmiR159b-PsMYB65 module functions in the resumption of bud growth after endodormancy by affecting the cell cycle in tree peony.

Bud endodormancy in perennial plants is a sophisticated system that adapts to seasonal climatic changes. Growth-promoting signals such as low temperature and gibberellins (GAs) are crucial for facilitating budbreak following endodormancy release (EDR). However, the regulatory mechanisms underlying GA-mediated budbreak in tree peony (Paeonia suffruticosa) remain unclear. In tree peony, the expression of PsmiR159b among three differentially expressed miR159 members was inhibited with the prolonged chilling, and overexpression of PsMIR159b delayed budbreak, whereas silencing PsmiR159b promoted budbreak after dormancy. PsMYB65, a downstream transcription factor in the GA pathway, was induced by prolonged chilling and exogenous GA3 treatments. PsMYB65 was identified as a target of PsmiR159b, and promoted budbreak in tree peony. RNA-seq of PsMYB65-slienced buds revealed significant enrichment in the GO terms regulation of 'cell cycle' and 'DNA replication' among differentially expressed genes. Yeast one-hybrid and electrophoretic mobility shift assays demonstrated that PsMYB65 directly bound to the promoter of the type-D cyclin gene PsCYCD3;1. Dual-luciferase reporter assay indicated that PsMYB65 positively regulate PsCYCD3;1 expression, suggesting that miR159b-PsMYB65 module contributes to budbreak by influencing the cell cycle. Our findings revealed that the PsmiR159b-PsMYB65 module functioned in budbreak after dormancy by regulating cell proliferation, providing valuable insights into the endodormancy release regulation mechanism.

Abscisic acid-induced transcription factor PsMYB306 negatively regulates tree peony bud dormancy release.

Bud dormancy is a crucial strategy for perennial plants to withstand adverse winter conditions. However, the regulatory mechanism of bud dormancy in tree peony (Paeonia suffruticosa) remains largely unknown. Here, we observed dramatically reduced and increased accumulation of abscisic acid (ABA) and bioactive gibberellins (GAs) GA1 and GA3, respectively, during bud endodormancy release of tree peony under prolonged chilling treatment. An Illumina RNA sequencing study was performed to identify potential genes involved in the bud endodormancy regulation in tree peony. Correlation matrix, principal component, and interaction network analyses identified a downregulated MYB transcription factor gene, PsMYB306, the expression of which positively correlated with 9-CIS-EPOXYCAROTENOID DIOXYGENASE 3 (PsNCED3) expression. Protein modeling analysis revealed 4 residues within the R2R3 domain of PsMYB306 to possess DNA binding capability. Transcription of PsMYB306 was increased by ABA treatment. Overexpression of PsMYB306 in petunia (Petunia hybrida) inhibited seed germination and plant growth, concomitant with elevated ABA and decreased GA contents. Silencing of PsMYB306 accelerated cold-triggered tree peony bud burst and influenced the production of ABA and GAs and the expression of their biosynthetic genes. ABA application reduced bud dormancy release and transcription of ENT-KAURENOIC ACID OXIDASE 1 (PsKAO1), GA20-OXIDASE 1 (PsGA20ox1), and GA3-OXIDASE 1 (PsGA3ox1) associated with GA biosynthesis in PsMYB306-silenced buds. In vivo and in vitro binding assays confirmed that PsMYB306 specifically transactivated the promoter of PsNCED3. Silencing of PsNCED3 also promoted bud break and growth. Altogether, our findings suggest that PsMYB306 negatively modulates cold-induced bud endodormancy release by regulating ABA production.

Bud endodormancy – a familiar but still unknown key adaptive trait in extratropical woody plants

In autumn, the buds of extratropical trees are in a state of endodormancy, since regardless of the prevailing environmental conditions, growth cannot be activated in these buds because the dormancy is caused by physiological factors in the buds. In natural conditions the growth-arresting physiological factors are removed by prolonged exposure to low chilling temperatures. This phenomenon is a key adaptive trait, for it prevents ‘false spring’, i.e., untimely bud burst during mild spells in autumn and winter, which would lead to cold damage during subsequent cold periods. Traditionally, endodormancy and the chilling requirement have been important in practical horticulture, as cultivars with low and high chilling requirements have been bred for locations in warm and cool climates, respectively. More recently, endodormancy and the chilling requirement have become major research themes in climate change studies where climatic change impacts are assessed by means of process-based tree phenology models. The dormancy phenomenon has been studied thoroughly at the whole-tree level for a hundred years, and several genes and genetic pathways involved have recently been identified in tree species such as hybrid aspen, apple, and pear. There is an urgent need, however, to integrate molecular physiological studies with modelling studies so as to understand the impact of climate change on the regulation of dormancy. To that end, we shall provide an overview of bud endodormancy research.

Temporal transcriptome and metabolite analyses provide insights into the biochemical and physiological processes underlying endodormancy release in pistachio (Pistacia vera L.) flower buds.

Pistachio (Pistacia vera L.), an economically and nutritionally important tree crop, relies on winter chill for bud endodormancy break and subsequent blooming and nut production. However, insufficient winter chill poses an increasing challenge in pistachio growing regions. To gain a better understanding of the physiological and biochemical responses of endodormant pistachio buds to chilling accumulation, we investigated the global gene expression changes in flower buds of pistachio cv. Kerman that were cultivated at three different orchard locations and exposed to increasing durations of winter chill. The expression of genes encoding β-1,3-glucanase and β-amylase, enzymes responsible for breaking down callose (β-1,3-glucan) and starch (α-1,4-glucan), respectively, increased during the endodormancy break of pistachio buds. This result suggested that the breakdown of callose obstructing stomata as well as the release of glucose from starch enables symplasmic trafficking and provides energy for bud endodormancy break and growth. Interestingly, as chilling accumulation increased, there was a decrease in the expression of nine-cis-epoxycarotenoid dioxygenase (NCED), encoding an enzyme that uses carotenoids as substrates and catalyzes the rate-limiting step in abscisic acid (ABA) biosynthesis. The decrease in NCED expression suggests ABA biosynthesis is suppressed, thus reducing inhibition of endodormancy break. The higher levels of carotenoid precursors and a decrease in ABA content in buds undergoing endodormancy break supports this suggestion. Collectively, the temporal transcriptome and biochemical analyses revealed that the degradation of structural (callose) and non-structural (starch) carbohydrates, along with the attenuation of ABA biosynthesis, are critical processes driving endodormancy break in pistachio buds.

Integrated genome-wide chromatin accessibility and expression profile identify key transcription factors involved in bud endodormancy break in tea plants

It is essential for tea plants (Camellia sinensis) to undergo bud endodormancy in order to survive winter and grow again the following spring. Molecular pathways underlying the release and break of endodormancy, however, remain unclear. Accessible chromatin regions play a crucial role in precise gene expression regulation. Here, we profiled the chromatin accessibility and transcriptional features of transcription factors (TFs) using ATAC- and RNA-seq technologies. We revealed dynamic changes during bud dormancy break in tea plants and detected open chromatin regions and TF binding sites. Numerous transcripts associated with open chromatin regions were found to exhibit dormant-preferential expression among TF-target genes. We focused on several crucial TF motifs, including MADS-box, AP2EREBP, bZIP, MYB, bHLH, E2FDP, REMB3, TCP, and G2-like factors, that were enriched in open chromatin regions at different budbreak stages, and predicted networks of TF-target genes. Then, we used qRT-PCR to investigate the expression patterns of budbreak-related genes.We found a set of differentially regulated peaks of MADS-box TFs and related genes enriched in plant hormone signal transduction pathway, photosynthesis, secondary metabolism, plant-pathogen interaction functions. Correlation analysis with the phytohormones abscisic acid and indole-3-acetic acid also provided details of the regulation network. Moreover, we identified the core TFs (SVP, CO, AP1, SOC, ABI, CBF, FRUITFULL, and ULTRAPETALA) of several pathways related to budbreak, providing the guideposts for future study.

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

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.

Cross‐disciplinary insights into the mechanisms of plant cold hardiness: From molecules to ecosystems

Cross‐disciplinary insights into the mechanisms of plant cold hardiness: From molecules to ecosystems

PpMAPK6 regulates peach bud endodormancy release through interactions with PpDAM6

The MADS-box (DAM) gene PpDAM6, which is related to dormancy, plays a key role in bud endodormancy release, and the expression of PpDAM6 decreases during endodormancy release. However, the interaction network that governs its regulation of the endodormancy release of flower buds in peach remains unclear. In this study, we used yeast two-hybrid (Y2H) assays to identify a mitogen-activated protein kinase, PpMAPK6, that interacts with PpDAM6 in a peach dormancy-associated SSHcDNA library. PpMAPK6 is primarily located in the nucleus, and Y2H and bimolecular fluorescence complementation (BiFC) assays verified that PpMAPK6 interacts with PpDAM6 by binding to the MADS-box domain of PpDAM6. Quantitative real-time PCR (qRT-PCR) analysis showed that the expression of PpMAPK6 was opposite that of PpDAM6 in the endodormancy release of three cultivars with different chilling requirements (Prunus persica ‘Chunjie’, Prunus persica var. nectarina ‘Zhongyou 5’, Prunus persica ‘Qingzhou peach’). In addition, abscisic acid (ABA) inhibited the expression of PpMAPK6 and promoted the expression of PpDAM6 in flower buds. The results indicated that PpMAPK6 might phosphorylate PpDAM6 to accelerate its degradation by interacting with PpDAM6. The expression of PpMAPK6 increased with decreasing ABA content during endodormancy release in peach flower buds, which in turn decreased the expression of PpDAM6 and promoted endodormancy release.

Comparative Study on Physiological Responses and Gene Expression of Bud Endodormancy Release Between Two Herbaceous Peony Cultivars (Paeonia lactiflora Pall.) With Contrasting Chilling Requirements.

With the global temperature increase, diverse endogenous factors and environmental cues can lead to severe obstacles to bud endodormancy release for important economic plants, such as herbaceous peony (Paeonia lactiflora Pall.). Knowing the underlying mechanism in bud endodormancy release is vital for widely planting herbaceous peony at low latitudes with warm winter climates. A systematic study was carried out between the southern Chinese cultivar ‘Hang Baishao’ with low-chilling requirement (CR) trait and the northern cultivar ‘Zhuguang’ with high-CR trait. Peony buds were sampled at regular intervals under natural cold during the crucial bud endodormancy release stage. Physiology and morphology of the buds were observed, and the roles of reactive oxygen species (ROS) and relevant genes in the regulation of bud endodormancy release were also highlighted, which has been rather rare in previous bud dormancy studies of both herbaceous and tree peonies. The expression of the starch metabolism- and sucrose synthesis-related genes PlAMY PlSPS and PlSUS was lower in the high-CR ‘Zhuguang’ and corresponded to a lower content of soluble sugars. The expression of polyamine oxidase gene PlPAO2 correlated with a higher level of hydrogen peroxide (H2O2) in high-CR ‘Zhuguang’ than in low CR ‘Hang Baishao’ during bud endodormancy. Expression of PlMAPKKK5, an intermediate gene in the abscisic acid (ABA) response to ROS signaling, correlated with ROS levels and ABA content. We present the hypothesis that accumulation of ROS increases ABA content and decreases GA3 content and signal transduction leading to reduced expression of PlSVP and PlSOC1. Reduced cell division and increased cellular damage which probably blocked bud endodormancy release were also observed in high-CR ‘Zhuguang’ through histological observation and related genes expression. This study provides a comparative analysis on physiological responses and gene expression patterns of bud dormancy of geophytes in an increasingly unsuitable environment.

Downregulation of lncRNA PpL-T31511 and Pp-miRn182 Promotes Hydrogen Cyanamide-Induced Endodormancy Release through the PP2C-H2O2 Pathway in Pear (Pyrus pyrifolia).

Bud endodormancy is an important, complex process subject to both genetic and epigenetic control, the mechanism of which is still unclear. The endogenous hormone abscisic acid (ABA) and its signaling pathway play important roles in the endodormancy process, in which the type 2C protein phosphatases (PP2Cs) is key to the ABA signal pathway. Due to its excellent effect on endodormancy release, hydrogen cyanamide (HC) treatment is considered an effective measure to study the mechanism of endodormancy release. In this study, RNA-Seq analysis was conducted on endodormant floral buds of pear (Pyrus pyrifolia) with HC treatment, and the HC-induced PP2C gene PpPP2C1 was identified. Next, software prediction, expression tests and transient assays revealed that lncRNA PpL-T31511-derived Pp-miRn182 targets PpPP2C1. The expression analysis showed that HC treatment upregulated the expression of PpPP2C1 and downregulated the expression of PpL-T31511 and Pp-miRn182. Moreover, HC treatment inhibited the accumulation of ABA signaling pathway-related genes and hydrogen peroxide (H2O2). Furthermore, overexpression of Pp-miRn182 reduced the inhibitory effect of PpPP2C1 on the H2O2 content. In summary, our study suggests that downregulation of PpL-T31511-derived Pp-miRn182 promotes HC-induced endodormancy release in pear plants through the PP2C-H2O2 pathway.

Dynamic of blueberry buds dormancy in a region of low chill occurrence

Several cultivars of blueberry were introduced in the colder regions in Brazil, but presented varied vegetative and reproductive growth, due to the heterogeneity of adaptation to the regional climate. The objective of this research was to determine the dormancy dynamics of blueberry buds grown in a region of low chill occurrence. Four methods of bud dormancy evaluation were used: biological test of single node cuttings, dormancy index, tetrazolium test and Tabuenca test. The dormancy of floral and vegetative buds of the cultivars Bluebelle, Climax, Delite and Powderblue of the Rabbiteye group was studied in collections every two weeks from April 26 to July 21. In the evaluated period there were only 76 h of temperatures below 7.2° C. The biological test and the dormancy index were viable methods for the dynamic evaluation of buds dormancy. The tetrazolium test was efficient to predict the exit of the endodormancy of floral and vegetative buds, but the Tabuenca test was efficient to predict the exit of floral buds dormancy only for the cultivars of less intense dormancy. The cultivars Bluebelle and Powderblue presented better adaptation to the conditions of low cold occurrence, with well defined installation and overcoming of the dormancy. The cv. Delite is more susceptible to budding heterogeneity and the cv. Climax is the least indicated to the region.

Endodormancy Release Can Be Modulated by the GA4-GID1c-DELLA2 Module in Peach Leaf Buds.

Gibberellin (GA) plays a key role in the release of bud dormancy and the GA receptor GID1 (GIBBERELLIN INSENSITIVE DWARF1) and DELLA protein are the GA signaling parts, but the molecular mechanism of GA-GID1-DELLA module regulating leaf bud dormancy in peach (Prunus persica) is still not very clear. In this study, we isolated and characterized the GID1 gene PpGID1c from the peach cultivar “Zhong you No.4.” Overexpressing PpGID1c in Arabidopsis promoted seed germination, which indicated that PpGID1c has an important function in dormancy. The expression level of PpGID1c in peach leaf buds during endodormancy release was higher than that during ecodormancy and was positively correlated with GA4 levels. Our study also found that GA4 had the most obvious effect on promoting the bud break, indicating that GA4 may be the key gibberellin to promoting peach leaf bud endodormancy release. Moreover, a quantitative real-time PCR (qRT-PCR) found that GA4 could increase the expression of the gibberellin signaling gene PpDELLA2. A yeast two-hybrid (Y2H) assay suggested that the PpGID1c interaction with the PpDELLA1 protein was not dependent on gibberellin, while the PpGID1c interaction with PpDELLA2 required GA4 or another gibberellin. These findings suggested that the GA4-GID1c-DELLA2 module regulates peach leaf bud endodormancy release, with this finding significantly enhancing our comprehensive understanding of bud endodormancy release and revealing a new mechanism for regulating leaf bud endodormancy release in peach.

Chilling and gibberellin acids hyperinduce β-1,3-glucanases to reopen transport corridor and break endodormancy in tree peony (Paeonia suffruticosa)

Bud endodormancy is accompanied by transport channel apertures blockage through callose deposition, and its resume to growth requires evoking β-1,3-glucanases (BGs) to unchoke the conduit. To understand out its working manner, the statuses of the transport channels were evaluated and candidate BGs were identified during chilling and gibberellin acids (GA) induced dormancy release in tree peony. Calcein reflects plasmodesmata permeability, and no calcein was observed in the bud together with density aniline blue fluorescent around the stem phloem at 0 d chilling. With the increase of chilling accumulation, the contents of glucan declined and the activities of gulcanase increased gradually in buds, and the calcein reached the top of flower primordia at 21 d chilled bud. Both GA3 and GA4 feedings promoted bud sprouting and growth along with rapidly unchoking the transport channels, and GA3 was more effective. Several candidate β-1,3-glucanase genes were detected, combining transcriptional profiling and quantitative PCR analysis. PsBG1, PsBG3, PsBG6, PsBG8 and PsBG9 were inducible by chilling accumulation and presented laminarin hydrolyzing activities after prokaryotically expression, while PsBG1, PsBG3, PsBG8 and PsBG9 responded to GAs application. Subcellular localizations revealed that PsBG6 and PsBG9 were plasmodesmata residents. It was concluded that PsBG6 played a vital role in chilling accumulation response and PsBG9 was central in GAs-induced dormancy release, and they could be used as marker genes for dormancy release in tree peony. These results were of great value to understand the mechanism of dormancy regulation and as an important fundamental for forcing culture technology in tree peony.