Transcriptomic Study of Early Responses to the Bud Dormancy-breaking Agent Hydrogen Cyanamide in ‘TropicBeauty’ Peach

To determine how the dormancy-breaking agent hydrogen cyanamide (HC) advances budbreak in peach (Prunus persica), this study compared the transcriptome of buds of low-chill ‘TropicBeauty’ peach trees treated with 1% (v/v) HC and that of nontreated trees at 3 and 7 days after treatment (DAT), respectively, using an RNA sequencing analysis. The peak of total budbreak occurred 6 weeks earlier in the HC-treated trees (at 32 DAT) than the nontreated trees (at 74 DAT). There were 1312 and 1095 differentially expressed genes (DEGs) at 3 and 7 DAT, respectively. At 3 DAT, DEGs related to oxidative stress, including the response to hypoxia, lipid oxidation, and reactive oxygen species (ROS) metabolic process, were upregulated in HC-treated buds. Additionally, DEGs encoding enzymes for ROS scavenging and the pentose phosphate pathway were upregulated at 3 DAT but they were not differently expressed at 7 DAT, indicating a temporary demand for defense mechanisms against HC-triggered oxidative stress. Upregulation of DEGs for cell division and development at 7 DAT, which were downregulated at 3 DAT, suggests that cell activity was initially suppressed but was enhanced within 7 DAT. At 7 DAT, DEGs related to cell wall degradation and modification were upregulated, which was possibly responsible for the burst of buds. The results of this study strongly suggest that HC induces transient oxidative stress shortly after application, leading to the release of bud dormancy and, subsequently, causing an increase in cell activity and cell wall loosening, thereby accelerating budbreak in peach.

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Effect of Defoliation Time on Depth of Dormancy and Bloom Time for Low-chill Peaches

HortScience ◽

10.21273/hortsci.25.12.1575 ◽

1990 ◽

Vol 25 (12) ◽

pp. 1575-1578 ◽

Cited By ~ 9

Author(s):

Jon Lloyd ◽

Daryl Firth

Keyword(s):

Prunus Persica ◽

Fruit Size ◽

Bud Dormancy ◽

Chilling Requirement ◽

Dormant Period ◽

Hydrogen Cyanamide ◽

Bud Development ◽

Dose Dependent ◽

Growth Ability

In a relatively low-chill environment, two cultivars of peach [Prunus persica (L.) Batsch] differing in chilling requirement (`Flordaprince', 150 units and `Flordagold', 325 units) were defoliated at 10-day intervals during midautumn. Effects of defoliation on depth of bud dormancy and dose-dependent responses of cuttings to hydrogen cyanamide throughout the dormant period were analyzed to develop a dormancy index (DI). DI values indicate that early defoliation reduces depth of bud dormancy throughout winter for both cultivars. For `Flordaprince', this was translated into early leafing and bloom, but fruit size was reduced by early relative to late defoliation. In contrast to `Flordaprince', vegetative and floral budbreak of `Flordagold' were delayed by early defoliation. These results indicate that early defoliation affects depth of dormancy and growth ability of buds, but that the extent to which these factors affect bud development depends on cultivar.

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191 SEASONAL VARIATION IN THE RESPONSE OF ENDODORMANT PEACH TO BIOREGULATORS AND THEIR INTERACTION WITH ETHYLENE

HortScience ◽

10.21273/hortsci.29.5.456d ◽

1994 ◽

Vol 29 (5) ◽

pp. 456d-456

Author(s):

William C. Mitchell ◽

Gregory A. Lang

Keyword(s):

Seasonal Variation ◽

Prunus Persica ◽

Tap Water ◽

Dormancy Breaking ◽

Hydrogen Cyanamide ◽

Silver Thiosulfate ◽

Cu Accumulation ◽

Temperature Regimes ◽

Growth Chambers ◽

Fall Application

Fall application of 2-chloroethylphosphoric acid (ethephon) is known to delay spring budbreak in peach (Prunus persica). To study seasonal variation in peach response to dormancy-breaking plant bioregulators and their possible interaction with ethylene, peach shoots were cut in the field at various intervals during endodormancy. Shoots were dipped in the dormancy-breaking bioregulators hydrogen cyanamide (H2CN2, 100 mM) or gibberellic acid (KGA3, 130 μm), alone or in combination with 1.38 mM ethephon. Treated shoots were held in beakers of either tap water or 1 mM silver thiosulfate (STS), and placed in growth chambers with potassium permanganate traps, 12/12 h photoperiods and 21/26 C temperature regimes. Dormancy-breaking efficacy (apical budbreak at 21 days) of both bioregulators increased as endodormancy progressed. At all intervals, H2CN2, broke dormancy more effectively than KGA3. The addition of ethephon to H2CN2 application prior to any CU accumulation (20 Oct) had no effect on efficacy (80% budbreak), but its addition after accumulation of ∼50 CU (8 Nov) or ∼320 CU (14 Dec) reduced subsequent budbreak to 25% and 40%, respectively. The addition of ethephon to KGA3 applications reduced budbreak both prior to (27 Oct) and after (8 Nov) initial CU accumulation. STS in the beaker solution increased both the extent (27 Oct) and the rate (14 Dec) of KGA-induced budbreak The interaction of ethylene, bioregulator type, and endodormancy regulation will be discussed.

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LncRNA SNHG12 Improves Cerebral Ischemic-reperfusion Injury by Activating SIRT1/FOXO3a Pathway through I nhibition of Autophagy and Oxidative Stress

Current Neurovascular Research ◽

10.2174/1567202617666200727142019 ◽

2020 ◽

Vol 17 (4) ◽

pp. 394-401

Author(s):

Yuanhua Wu ◽

Yuan Huang ◽

Jing Cai ◽

Donglan Zhang ◽

Shixi Liu ◽

...

Keyword(s):

Oxidative Stress ◽

Molecular Mechanisms ◽

Ischemia Reperfusion ◽

Critical Role ◽

Cell Activity ◽

Ht22 Cells ◽

Cerebral Ischemic ◽

Cerebral Ischemic Reperfusion ◽

And Oxidative Stress

Background: Ischemia/reperfusion (I/R) injury involves complex biological processes and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury. Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway. In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression was down-regulated in HT22 cells of I/R model. Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition, the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12 group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased the I/R induced release of ROS and MDA. Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model. This study might provide new potential therapeutic targets for further investigating the mechanisms in cerebral I/R injury and provide.

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Systematic Identification of Regulators of Oxidative Stress Reveals Non-canonical Roles for Peroxisomal Import and the Pentose Phosphate Pathway

Cell Reports ◽

10.1016/j.celrep.2020.01.013 ◽

2020 ◽

Vol 30 (5) ◽

pp. 1417-1433.e7 ◽

Cited By ~ 7

Author(s):

Michael M. Dubreuil ◽

David W. Morgens ◽

Kanji Okumoto ◽

Masanori Honsho ◽

Kévin Contrepois ◽

...

Keyword(s):

Oxidative Stress ◽

Pentose Phosphate Pathway ◽

Pentose Phosphate ◽

Systematic Identification

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Interplay among Antioxidant System, Hormone Profile and Carbohydrate Metabolism during Bud Dormancy Breaking in a High-Chill Peach Variety

Antioxidants ◽

10.3390/antiox10040560 ◽

2021 ◽

Vol 10 (4) ◽

pp. 560

Author(s):

José A. Hernández ◽

Pedro Díaz-Vivancos ◽

José Ramón Acosta-Motos ◽

Nuria Alburquerque ◽

Domingo Martínez ◽

...

Keyword(s):

Starch Content ◽

Sugar Metabolism ◽

Bud Dormancy ◽

Dormancy Breaking ◽

Prunus Species ◽

Physiological Factors ◽

Antioxidant Metabolism ◽

Hormone Profile ◽

Aba Content ◽

Gas Ratio

(1) Background: Prunus species have the ability to suspend (induce dormancy) and restart growth, in an intricate process in which environmental and physiological factors interact. (2) Methods: In this work, we studied the evolution of sugars, antioxidant metabolism, and abscisic acid (ABA) and gibberellins (GAs) levels during bud dormancy evolution in a high-chill peach variety, grown for two seasons in two different geographical areas with different annual media temperature, a cold (CA) and a temperate area (TA). (3) Results: In both areas, starch content reached a peak at ecodormancy, and then decreased at dormancy release (DR). Sorbitol and sucrose declined at DR, mainly in the CA. In contrast, glucose and fructose levels progressively rose until DR. A decline in ascorbate peroxidase, dehydroascorbate reductase, superoxide dismutase and catalase activities occurred in both seasons at DR. Moreover, the H2O2-sensitive SOD isoenzymes, Fe-SOD and Cu,Zn-SOD, and two novel peroxidase isoenzymes, were detected. Overall, these results suggest the occurrence of a controlled oxidative stress during DR. GA7 was the major bioactive GA in both areas, the evolution of its levels being different between seasons and areas. In contrast, ABA content decreased during the dormancy period in both areas, resulting in a reduction in the ABA/total GAs ratio, being more evident in the CA. (4) Conclusion: A possible interaction sugars-hormones-ROS could take place in high-chill peach buds, favoring the DR process, suggesting that, in addition to sugar metabolism, redox interactions can govern bud DR, regardless of chilling requirements.

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The Remarkable Antioxidant and Anti-Inflammatory Potential of the Extracts of the Brown Alga Cystoseira amentacea var. stricta

Marine Drugs ◽

10.3390/md19010002 ◽

2020 ◽

Vol 19 (1) ◽

pp. 2

Author(s):

Gina De La Fuente ◽

Marco Fontana ◽

Valentina Asnaghi ◽

Mariachiara Chiantore ◽

Serena Mirata ◽

...

Keyword(s):

Oxidative Stress ◽

No Production ◽

Low Grade ◽

Raw 264.7 ◽

Ros Scavenging ◽

Ligurian Sea ◽

Raw 264.7 Macrophages ◽

Pharmaceutical Industries ◽

Anti Inflammatory ◽

First Time

Inflammation and oxidative stress are part of the complex biological responses of body tissues to harmful stimuli. In recent years, due to the increased understanding that oxidative stress is implicated in several diseases, pharmaceutical industries have invested in the research and development of new antioxidant compounds, especially from marine environment sources. Marine seaweeds have shown the presence of many bioactive secondary metabolites, with great potentialities from both the nutraceutical and the biomedical point of view. In this study, 50%-ethanolic and DMSO extracts from the species C. amentacea var. stricta were obtained for the first time from seaweeds collected in the Ligurian Sea (north-western Mediterranean). The bioactive properties of these extracts were then investigated, in terms of quantification of specific antioxidant activities by relevant ROS scavenging spectrophotometric tests, and of anti-inflammatory properties in LPS-stimulated macrophages by evaluation of inhibition of inflammatory cytokines and mediators. The data obtained in this study demonstrate a strong anti-inflammatory effect of both C. amentacea extracts (DMSO and ethanolic). The extracts showed a very low grade of toxicity on RAW 264.7 macrophages and L929 fibroblasts and a plethora of antioxidant and anti-inflammatory effects that were for the first time thoroughly investigated. The two extracts were able to scavenge OH and NO radicals (OH EC50 between 392 and 454 μg/mL; NO EC50 between 546 and 1293 μg/mL), to partially rescue H2O2-induced RAW 264.7 macrophages cell death, to abate intracellular ROS production in H2O2-stimulated macrophages and fibroblasts and to strongly inhibit LPS-induced inflammatory mediators, such as NO production and IL-1α, IL-6, cyclooxygenase-2 and inducible NO synthase gene expression in RAW 264.7 macrophages. These results pave the way, for the future use of C. amentacea metabolites, as an example, as antioxidant food additives in antiaging formulations as well as in cosmetic lenitive lotions for inflamed and/or damaged skin.

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THE EFFECT OF CONCENTRATIONS AND APPLICATION OF HYDROGEN CYANAMIDE ON KIWIFRUIT DORMANCY BREAKING

Acta Horticulturae ◽

10.17660/actahortic.1995.395.19 ◽

1995 ◽

pp. 177-184 ◽

Cited By ~ 8

Author(s):

E. Schuck ◽

J.L. Petri

Keyword(s):

Dormancy Breaking ◽

Hydrogen Cyanamide

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TIGAR regulates glycolysis in ischemic kidney proximal tubules

AJP Renal Physiology ◽

10.1152/ajprenal.00459.2014 ◽

2015 ◽

Vol 308 (4) ◽

pp. F298-F308 ◽

Cited By ~ 25

Author(s):

Jinu Kim ◽

Kishor Devalaraja-Narashimha ◽

Babu J. Padanilam

Keyword(s):

Oxidative Stress ◽

Reperfusion Injury ◽

Pentose Phosphate Pathway ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Pentose Phosphate ◽

Atp Depletion ◽

G6pd Activity ◽

Histological Damage ◽

Severe Ischemia

Tp53-induced glycolysis and apoptosis regulator (TIGAR) activation blocks glycolytic ATP synthesis by inhibiting phosphofructokinase-1 activity. Our data indicate that TIGAR is selectively induced and activated in renal outermedullary proximal straight tubules (PSTs) after ischemia-reperfusion injury in a p53-dependent manner. Under severe ischemic conditions, TIGAR expression persisted through 48 h postinjury and induced loss of renal function and histological damage. Furthermore, TIGAR upregulation inhibited phosphofructokinase-1 activity, glucose 6-phosphate dehydrogenase (G6PD) activity, and induced ATP depletion, oxidative stress, autophagy, and apoptosis. Small interfering RNA-mediated TIGAR inhibition prevented the aforementioned malevolent effects and protected the kidneys from functional and histological damage. After mild ischemia, but not severe ischemia, G6PD activity and NADPH levels were restored, suggesting that TIGAR activation may redirect the glycolytic pathway into gluconeogenesis or the pentose phosphate pathway to produce NADPH. The increased level of NADPH maintained the level of GSH to scavenge ROS, resulting in a lower sensitivity of PST cells to injury. Under severe ischemia, G6PD activity and NADPH levels were reduced during reperfusion; however, blockade of TIGAR enhanced their levels and reduced oxidative stress and apoptosis. Collectively, these results demonstrate that inhibition of TIGAR may protect PST cells from energy depletion and apoptotic cell death in the setting of severe ischemia-reperfusion injury. However, under low ischemic burden, TIGAR activation induces the pentose phosphate pathway and autophagy as a protective mechanism.

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