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BACKGROUND: Melatonin, a hormone present in animals and some plants, has garnered attention for its potential in preserving harvested produce. Softening due to changes in cell wall composition and wilting caused by weight loss are the major reasons for the loss of commercial value in postharvest okra. This study aimed to evaluate the impact of melatonin on the softening and weight loss of postharvest okra. RESULTS: The results revealed that the application of melatonin had a significant influence on the maintenance of fruit firmness by inhibiting the breakdown and dissolution of cell wall polysaccharides by suppressing the expression of specific genes responsible for cell wall degradation in okra. Conversely, melatonin treatment positively influenced the expression of genes involved in the synthesis of cell wall components. Furthermore, the treatment exhibited notable benefits in reducing weight loss in okra, which was accomplished by promoting the closure of stomata - the tiny pores on the surface of the fruit. CONCLUSION: Melatonin could serve as a novel approach to reduce water loss, delay fruit softening and extend the shelf life of okra. © 2024 Society of Chemical Industry.
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The effects of γ-aminobutyric (GABA) on enzymatic browning, storage quality, membrane and reactive oxygen species (ROS) metabolism in fresh-cut stem lettuce were investigated. The results illustrated that GABA treatment delayed browning degree, polyphenol oxidase (PPO) activity and the expression of LsPPO. Meanwhile, higher chlorophyll and ascorbic acid contents were exhibited in GABA-treated stem lettuce, as well as the slower microbial propagation. Further investigation revealed that exogenous GABA application declined malondialdehyde content, electrolyte leakage and the enzyme activities of membrane metabolism, and the expression levels of related genes were also downregulated. In addition, GABA treatment scavenged ROS and strengthened the enzyme activities of ROS metabolism, as well as the expression levels of corresponding genes. Taken together, these findings implied that the repressed enzymatic browning and microbial propagation in GABA-treated stem lettuce were due to the inhibition of ROS accumulation, enhancement of membrane stability and increased resistance to oxidation.
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Programmed cell death (PCD) is a genetically regulated process of cell suicide essential for plant development. The 'malate valve' is a mechanism that ensures redox balance across different subcellular compartments. In broccoli, the BomMDH1 gene encodes malate dehydrogenase in mitochondria, a critical enzyme in the 'malate circulation' pathway. This study investigates the functional role of BomMDH1 in malate (MA)-induced apoptosis in bright yellow-2 (BY-2) suspension cells. Findings revealed that transgenic cells overexpressing BomMDH1 showed enhanced viability under MA-induced oxidative stress compared to wild-type (WT) cells. Overexpression of BomMDH1 also reduced levels of reactive oxygen species (ROS), hydrogen peroxide (H2O2), and malondialdehyde (MDA), while increasing the expression of antioxidant enzyme genes such as NtAPX, NtAOX1a, NtSOD, and NtMDHAR. Additionally, treatment with salicylhydroxamic acid (SHAM), a characteristic inhibitor of mitochondrial respiration, further improved the anti-apoptotic activity of BY-2 cells. Overall, these results highlighted the function of the BomMDH1 gene and the potential of SHAM treatment in mitigating oxidative stress in BY-2 suspension cells.
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Malatos , Nicotiana , Estrés Oxidativo , Especies Reactivas de Oxígeno , Estrés Oxidativo/efectos de los fármacos , Malatos/metabolismo , Nicotiana/genética , Nicotiana/efectos de los fármacos , Especies Reactivas de Oxígeno/metabolismo , Apoptosis/efectos de los fármacos , Peróxido de Hidrógeno/metabolismo , Proteínas de Plantas/metabolismo , Proteínas de Plantas/genética , Malato Deshidrogenasa/metabolismo , Malato Deshidrogenasa/genética , Mitocondrias/metabolismo , Malondialdehído/metabolismo , Regulación de la Expresión Génica de las PlantasRESUMEN
Carotenoid oxidative cleavage is a significant factor contributing to the color changes of shredded carrots and treatment with calcium chloride (CaCl2, 1% w/v) has been observed to alleviate the whitening symptom and color loss. However, the specific mechanism by which CaCl2 treatment suppresses carotenoid degradation remains unclear. In this study, the effect of CaCl2 and EGTA (calcium ion chelating agent) treatment on carotenoid biosynthesis and degradation in shredded carrots and the mechanism involved was investigated. CaCl2 treatment promoted the expression and activity of carotenoid biosynthetic enzyme (phytoene synthase, PSY), but inhibited the increases of the degradative enzyme activity of carotenoid cleavage dioxygenase (CCD) and down-regulated the corresponding transcripts, thus delayed the degradation of total carotenoid and maintaining higher levels of major carotenoid compounds including ß-carotene, α-carotene, lycopene, and lutein in shredded carrots during storage. However, EGTA treatment promoted the gene expression and enzyme activity of CCD and increased the degradation of carotenoid compounds in shredded carrots during storage. Furthermore, the CaCl2 treatment induced DcCAMTA4, identified as a calcium decoder in shredded carrots, which, in turn, suppressed the expressions of DcCCD1 and DcCCD4 by interacting with their promoters. The transient overexpression of DcCAMTA4 in tobacco leaves led to reduced expression of NtCCD1 and NtCCD4, maintaining a higher content of carotenoids. Thus, CaCl2 alleviated the oxidative cleavage of carotenoids in shredded carrots through the DcCAMTA4-mediated carotenoid degradation pathway.
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Cloruro de Calcio , Carotenoides , Daucus carota , Proteínas de Plantas , Carotenoides/metabolismo , Cloruro de Calcio/farmacología , Daucus carota/metabolismo , Daucus carota/genética , Proteínas de Plantas/metabolismo , Proteínas de Plantas/genética , Regulación de la Expresión Génica de las Plantas/efectos de los fármacos , Oxidación-Reducción/efectos de los fármacosRESUMEN
BACKGROUND: Dysregulation of vascular smooth muscle cell (VSMC) function leads to a variety of diseases such as atherosclerosis and hyperplasia after injury. However, antiproliferative drug targeting VSMC exhibits poor specificity. Therefore, there is an urgent to develop highly specific antiproliferative drugs to prevention and treatment VSMC dedifferentiation associated arteriosclerosis. Kanglexin (KLX), a new anthraquinone compound designed by our team, has potential to regulate VSMC phenotype according to the physicochemical properties. PURPOSE: This project aims to evaluate the therapeutic role of KLX in VSMC dedifferentiation and atherosclerosis, neointimal formation and illustrates the underlying molecular mechanism. METHODS: In vivo, the ApoE-/- mice were fed with high-fat diet (HFD) for a duration of 13 weeks to establish the atherosclerotic model. And rat carotid artery injury model was performed to establish the neointimal formation model. In vitro, PDGF-BB was used to induce VSMC dedifferentiation. RESULTS: We found that KLX ameliorated the atherosclerotic progression including atherosclerotic lesion formation, lipid deposition and collagen deposition in aorta and aortic sinus in atherosclerotic mouse model. In addition, The administration of KLX effectively ameliorated neointimal formation in the carotid artery following balloon injury in SD rats. The findings derived from molecular docking and surface plasmon resonance (SPR) experiments unequivocally demonstrate that KLX had potential to bind PDGFR-ß. Mechanism research work proved that KLX prevented VSMC proliferation, migration and dedifferentiation via activating the PDGFR-ß-MEK -ERK-ELK-1/KLF4 signaling pathway. CONCLUSION: Collectively, we demonstrated that KLX effectively attenuated the progression of atherosclerosis in ApoE-/- mice and carotid arterial neointimal formation in SD rats by inhibiting VSMC phenotypic conversion via PDGFR-ß-MEK-ERK-ELK-1/KLF4 signaling. KLX exhibits promising potential as a viable therapeutic agent for the treatment of VSMC phenotype conversion associated arteriosclerosis.
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Antraquinonas , Desdiferenciación Celular , Factor 4 Similar a Kruppel , Músculo Liso Vascular , Neointima , Animales , Masculino , Ratones , Ratas , Antraquinonas/farmacología , Arteriosclerosis/tratamiento farmacológico , Arteriosclerosis/prevención & control , Aterosclerosis/tratamiento farmacológico , Becaplermina/farmacología , Traumatismos de las Arterias Carótidas/tratamiento farmacológico , Desdiferenciación Celular/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Dieta Alta en Grasa , Modelos Animales de Enfermedad , Factores de Transcripción de Tipo Kruppel/metabolismo , Ratones Endogámicos C57BL , Simulación del Acoplamiento Molecular , Músculo Liso Vascular/efectos de los fármacos , Miocitos del Músculo Liso/efectos de los fármacos , Neointima/tratamiento farmacológico , Ratas Sprague-Dawley , Receptores del Factor de Crecimiento Derivado de Plaquetas/metabolismo , Transducción de Señal/efectos de los fármacosRESUMEN
The rapid activation of phosphatidylinositol-specific phospholipase C (PI-PLC) occurs early after the stimulation of biotic and abiotic stress in plants, which directly associated with the calcium channel-induced calcium ion (Ca2+) influx. Exogenous calcium chloride (CaCl2) mediates the calcium signaling transduction to promote the γ-aminobutyric acid accumulation and nutritional quality in shredded carrots whereas the generation mechanism remains uncertain. Therefore, the involvement of PI-PLC-associated phospholipid metabolism was investigated in present study. Our result revealed that CaCl2 treatment promoted the expression and activity of PI-PLC and increased the inositol 1,4,5-trisphosphate and hexakisphosphate content in shredded carrots. The transcripts of multi-glutamate receptor-like channels (DcGLRs), the glutamate and γ-aminobutyric acid (GABA) content, and Ca2+ influx were induced by CaCl2 treatment in shredded carrots during storage. However, PI-PLC inhibitor (U73122) treatment inhibited the activation of PI-PLC, the increase of many DcGLRs family genes expression levels, and Ca2+ influx. Moreover, the identification of DcPI-PLC4/6 and DcGLRs proteins, along with the analysis of characteristic domains such as PLCXc, PLCYc, C2 domain, transmembranous regions, and ligand binding domain, suggests their involvement in phospholipid catalysis and calcium transport in carrots. Furthermore, DcPI-PLC4/6 overexpression in tobacco leaves induced the Ca2+ influx by activating the expressions of NtGLRs and the accumulation of glutamate and GABA. These findings collectively indicate that CaCl2 treatment-induced PI-PLC activation influences DcGLRs expression levels to mediate cytosolic Ca2+ influx, thus, highlighting the "PI-PLC-GLRs-Ca2+" pathway in calcium signaling generation and GABA biosynthesis in shredded carrots.
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Cloruro de Calcio , Calcio , Daucus carota , Fosfolípidos , Calcio/metabolismo , Daucus carota/metabolismo , Daucus carota/efectos de los fármacos , Cloruro de Calcio/farmacología , Fosfolípidos/metabolismo , Fosfoinositido Fosfolipasa C/metabolismo , Regulación de la Expresión Génica de las Plantas/efectos de los fármacos , Proteínas de Plantas/metabolismo , Proteínas de Plantas/genéticaRESUMEN
Phenotype transformation of vascular smooth muscle cells (VSMCs) plays an important role in the development of atherosclerosis. Asprosin is a newly discovered adipokine, which is critical in regulating metabolism. However, the relationship between asprosin and phenotype transformation of VSMCs in atherosclerosis remains unclear. The aim of this study is to investigate whether asprosin affects the progression of atherosclerosis by inducing phenotype transformation of VSMCs. We established an atherosclerosis model in ApoE-/- mice and administered asprosin recombinant protein and asprosin antibody to mice. Knocking down asprosin was also as an intervention. Interestingly, we found a correlation between asprosin levels and atherosclerosis. Asprosin promoted plaque formation and phenotype transformation of VSMCs. While, AspKD or asprosin antibody reduced the plaque lesion and suppressed vascular stiffness in ApoE-/- mice. Mechanistically, asprosin induced phenotype transformation of MOVAs by binding to GPR54, leading to Gαq/11 recruitment and activation of the PLC-PKC-ERK1/2-STAT3 signaling pathway. Si GPR54 or GPR54 antagonist partially inhibited the action of asprosin in MOVAs. Mutant GPR54-(267, 307) residue cancelled the binding of asprosin and GPR54. In summary, this study confirmed asprosin activated GPR54/Gαq/11-dependent ERK1/2-STAT3 signaling pathway, thereby promoting VSMCs phenotype transformation and aggravating atherosclerosis, thus providing a new target for the treatment of atherosclerosis.
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Aterosclerosis , Músculo Liso Vascular , Miocitos del Músculo Liso , Fenotipo , Animales , Aterosclerosis/metabolismo , Aterosclerosis/patología , Aterosclerosis/genética , Músculo Liso Vascular/metabolismo , Músculo Liso Vascular/patología , Ratones , Miocitos del Músculo Liso/metabolismo , Miocitos del Músculo Liso/patología , Fibrilina-1/metabolismo , Fibrilina-1/genética , Receptores Acoplados a Proteínas G/metabolismo , Receptores Acoplados a Proteínas G/genética , Masculino , Transducción de Señal , Modelos Animales de Enfermedad , Apolipoproteínas E/deficiencia , Apolipoproteínas E/genética , Apolipoproteínas E/metabolismo , Humanos , Proteínas de la Matriz Extracelular/metabolismo , Proteínas de la Matriz Extracelular/genética , Ratones NoqueadosRESUMEN
It is well established that programmed cell death (PCD) occurred in broccoli during postharvest senescence, but no studies have been conducted on the regulation of broccoli cytochrome f by mannose treatment and its relationship with PCD. In this study, we treated broccoli buds with mannose to investigate the changes in color, total chlorophyll content, gene expression related to chlorophyll metabolism, chloroplast structure, and cytochrome f determination during postharvest storage. In addition, to investigate the effect of cytochrome f on PCD, we extracted cytochrome f from broccoli and treated Nicotiana tabacum L. cv Bright Yellow 2 (BY-2) cells with extracted cytochrome f from broccoli at various concentrations. The results showed that cytochrome f can induce PCD in tobacco BY-2 cells, as evidenced by altered cell morphology, nuclear chromatin disintegration, DNA degradation, decreased cell viability, and increased caspase-3-like protease production. Taken together, our study indicated that mannose could effectively delay senescence of postharvest broccoli by inhibiting the expression of gene encoding cytochrome f which could induce PCD.
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Brassica , Brassica/genética , Citocromos f/metabolismo , Manosa/metabolismo , Manosa/farmacología , Nicotiana/genética , Apoptosis , Clorofila/metabolismoRESUMEN
Fresh-cut potatoes are prone to surface browning and physiological degradation. Chlorogenic acid (CGA), a natural phenolic antioxidant, has demonstrated preservative properties in various postharvest products. However, the underlying mechanisms of its application on maintaining quality remain unclear. Therefore, the effect of exogenous CGA treatment on quality deterioration of potato slices and the mechanisms involved were investigated. Results revealed CGA treatment retarded the browning coloration, suppressed microbial growth and inhibited the declines in starch, and ascorbic acid contents in potato slices. Meanwhile, the treatment activated the phenylpropanoid pathway but decreased the activities of phenolic decomposition-related enzymes such as polyphenol oxidase (PPO) and tyrosinase and downregulated StPPO expression. Moreover, the treated slices exhibited reduced accumulation of reactive oxygen species and increased activity of antioxidant enzymes. Additionally, they displayed enhanced 2,2-diphenyl-1-picrylhydrazyl radicals scavenging capacity and higher ATP levels. Therefore, these findings indicated that CGA treatment was effective for quality maintenance and antioxidant capacity enhancement in fresh-cut potatoes, thereby providing potential strategies for the preservation and processing of fresh-cut produce.
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Antioxidantes , Solanum tuberosum , Antioxidantes/metabolismo , Ácido Clorogénico/farmacología , Ácido Clorogénico/metabolismo , Solanum tuberosum/metabolismo , Fenoles/metabolismo , Ácido Ascórbico/metabolismo , Catecol Oxidasa/metabolismoRESUMEN
Okra has been widely cultivated worldwide. Consumers appreciate its nutritional value and delicious taste. However, okra is very perishable after harvest because of rapid senescence and high susceptibility to mechanical injuries, which limits its storage life and reduces consumer acceptance. This study examined the influence of melatonin treatment on senescence process and endogenous plant signalling molecules in postharvest okras. The results indicated that melatonin treatment delayed senescence by increasing the endogenous melatonin content through upregulation of its biosynthetic genes. In addition, the treatment increased the contents of indole-3-acetic acid (IAA) and gibberellin (GA) due to the positive modulation of their metabolic and signalling genes. Furthermore, treated okras exhibited higher levels of γ-aminobutyric acid (GABA) but lower abscisic acid (ABA) content, contributing to the delayed senescence process compared to control. Overall, the findings suggested that melatonin postponed senescence in okras fruit by positively regulating endogenous signalling molecules such as melatonin, IAA, GABA, GA, and ABA.
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The effects of exogenous glutamate treatment on the quality attributes, γ-aminobutyric acid (GABA) shunt, phenylpropanoid pathway, and antioxidant capacity of fresh-cut carrots were investigated. Results showed that glutamate treatment suppressed the increases in lightness and whiteness values, inhibited the degradation of total carotenoids and maintained better flavor and taste in fresh-cut carrots. Moreover, glutamate treatment rapidly promoted the activities of glutamate decarboxylase and GABA transaminase, thus improving the GABA content. It also significantly enhanced the activities of phenylalanine ammonia-lyase, cinnamate-4-hydroxylase, and 4-coumarate coenzyme A ligase and promoted the accumulation of total phenolics as well as the main individual phenolic compounds, including chlorogenic and caffeic acid. In addition, glutamate application activated the reactive oxygen system-related enzyme including peroxidase, superoxide dismutase, ascorbate peroxidase, and catalase activities to maintain higher antioxidant capacity in fresh-cut carrots. These results demonstrated that exogenous glutamate treatment maintained better nutritional quality and alleviated color deterioration by accelerating the accumulation of GABA and phenolics and enhancing the antioxidant capacity in fresh-cut carrots.
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Antioxidantes , Daucus carota , Antioxidantes/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Daucus carota/metabolismo , Ácido Glutámico/metabolismo , Ácido gamma-Aminobutírico/metabolismoRESUMEN
Lung cancer is a leading cause of cancer-related deaths worldwide. Recent studies have identified pyroptosis, a type of programmed cell death, as a critical process in the development and progression of lung cancer. In this study, we investigated the effect of EEBR, a new compound synthesized by our team, on pyroptosis in non-small cell lung cancer cells (NSCLC) and the underlying molecular mechanisms. Our results demonstrated that EEBR significantly reduced the proliferation and metastasis of NSCLC cells in vitro. Moreover, EEBR-induced pyroptosis in NSCLC cells, as evidenced by cell membrane rupture, the release of cytokines such as interleukin-18 and interleukin-1 beta and the promotion of Gasdermin D cleavage in a Caspase-1-dependent manner. Furthermore, EEBR promoted the nuclear translocation of NF-κB and upregulated the protein level of NLRP3. Subsequent studies revealed that EEBR-induced pyroptosis was suppressed by the inhibition of NF-κB. Finally, EEBR effectively suppressed the growth of lung cancer xenograft tumours by promoting NSCLC pyroptosis in animal models. Taken together, our findings suggest that EEBR induces Caspase-1-dependent pyroptosis through the NF-κB/NLRP3 signalling cascade in NSCLC, highlighting its potential as a candidate drug for NSCLC treatment.
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Carcinoma de Pulmón de Células no Pequeñas , Neoplasias Pulmonares , Animales , Humanos , FN-kappa B/metabolismo , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Carcinoma de Pulmón de Células no Pequeñas/patología , Piroptosis , Caspasa 1/metabolismo , Inflamasomas/metabolismoRESUMEN
Restenosis after angioplasty is caused usually by neointima formation characterized by aberrant vascular smooth muscle cell (VSMC) dedifferentiation. Myeloid-derived growth factor (MYDGF), secreted from bone marrow-derived monocytes and macrophages, has been found to have cardioprotective effects. In this study we investigated the effect of MYDGF to postinjury neointimal formation and the underlying mechanisms. Rat carotid arteries balloon-injured model was established. We found that plasma MYDGF content and the level of MYDGF in injured arteries were significantly decreased after balloon injury. Local application of exogenous MYDGF (50 µg/mL) around the injured vessel during balloon injury markedly ameliorated the development of neointimal formation evidenced by relieving the narrow endovascular diameter, improving hemodynamics, and reducing collagen deposition. In addition, local application of MYDGF inhibited VSMC dedifferentiation, which was proved by reversing the elevated levels of osteopontin (OPN) protein and decreased levels of α-smooth muscle actin (α-SMA) in the left carotid arteries. We showed that PDGF-BB (30 ng/mL) stimulated VSMC proliferation, migration and dedifferentiation in vitro; pretreatment with MYDGF (50-200 ng/mL) concentration-dependently eliminated PDGF-BB-induced cell proliferation, migration and dedifferentiation. Molecular docking revealed that MYDGF had the potential to bind with sphingosine-1-phosphate receptor 2 (S1PR2), which was confirmed by SPR assay and Co-IP analysis. Pretreatment with CCG-1423 (Rho signaling inhibitor), JTE-013 (S1PR2 antagonist) or Ripasudil (ROCK inhibitor) circumvented the inhibitory effects of MYDGF on VSMC phenotypic switching through inhibiting S1PR2 or its downstream RhoA-actin monomers (G-actin) /actin filaments (F-actin)-MRTF-A signaling. In summary, this study proves that MYDGF relieves neointimal formation of carotid arteries in response to balloon injury in rats, and suppresses VSMC dedifferentiation induced by PDGF-BB via S1PR2-RhoA-G/F-actin-MRTF-A signaling pathway. In addition, our results provide evidence for cross talk between bone marrow and vasculature.
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Actinas , Neointima , Ratas , Animales , Becaplermina/farmacología , Neointima/tratamiento farmacológico , Neointima/metabolismo , Actinas/metabolismo , Ratas Sprague-Dawley , Receptores de Esfingosina-1-Fosfato/metabolismo , Factor Estimulante de Colonias de Granulocitos/metabolismo , Factor Estimulante de Colonias de Granulocitos/farmacología , Músculo Liso Vascular , Simulación del Acoplamiento Molecular , Proliferación Celular , Transducción de Señal , Movimiento Celular , Miocitos del Músculo Liso/metabolismo , Células CultivadasRESUMEN
The effect of calcium chloride (CaCl2) treatment on γ-aminobutyric acid (GABA) accumulation in fresh-cut cantaloupe and the involved mechanisms were investigated. The result showed that 1% (w/v) CaCl2 treatment increased GABA content and activities of glutamate decarboxylase (GAD) and succinate semialdehyde dehydrogenase (SSADH), while decreased glutamate (Glu) content and GABA transaminase (GABA-T) activities in fresh-cut cantaloupe. CmCML11 and CmCAMTA5 expressions of CaCl2-treated fruit increased by 187.4% and 165.6% than control fruit in the initial 6 h. Besides, expressions of GABA shunt genes, including CmGAD1, CmGAD2, CmGABA-T and CmSSADH were also up-regulated by CaCl2 treatment during early storage. Moreover, acting as a transcriptional activator, CmCAMTA5 could bind to the CG-box in promoters of CmGAD1, CmGABA-T and CmSSADH and activate their transcription. Furthermore, the interaction between CmCML11 and CmCAMTA5 could enhance the transcriptional activation on GABA shunt genes which were regulated by CmCAMTA5. Collectively, our findings revealed that CaCl2 treatment promoted GABA accumulation in fresh-cut cantaloupe via the combined effect of CmCML11 and CmCAMTA5 in the regulation of expressions of CmGAD1, CmGABA-T, and CmSSADH in GABA shunt.
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Cucumis melo , Cucumis melo/genética , Cucumis melo/metabolismo , Cloruro de Calcio , 4-Aminobutirato Transaminasa/genética , 4-Aminobutirato Transaminasa/metabolismo , Ácido gamma-Aminobutírico/metabolismo , Ácido GlutámicoRESUMEN
Fruits are highly recommended nowadays in human diets because they are rich in vitamins, minerals, fibers and other necessary nutrients. The final stage of fruit production, known as ripening, plays a crucial role in determining the fruit's quality and commercial value. This is a complex physiological process, which involves many phytohormones and regulatory factors. Among the phytohormones involved in fruit ripening, abscisic acid (ABA) holds significant importance. ABA levels generally increase during the ripening process in most fruits, and applying ABA externally can enhance fruit flavor, hasten softening, and promote color development through complex signal regulation. Therefore, gaining a deeper understanding of ABA's mechanisms in fruit ripening is valuable for regulating various fruit characteristics, making them more suitable for consumption or storage. This, in turn, can generate greater economic benefits and reduce postharvest losses. This article provides an overview of the relationship between ABA and fruit ripening. It summarizes the effects of ABA on ripening related traits, covering the biochemical aspects and the underlying molecular mechanisms. Additionally, the article discusses the interactions of ABA with other phytohormones during fruit ripening, especially ethylene, and provides perspectives for future exploration in this field.
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The widespread application of copper (Cu) -based fertilizers and pesticides could increase the accumulation of Cu in kiwifruit. According to a global survey, red- and yellow-fleshed kiwifruit contained more elevated amounts of Cu than green-fleshed kiwifruit due to weaker disease resistance and higher use of Cu pesticides. Intriguingly, our research revealed that external and endogenous ascorbic acid (AsA) reduced the phenotypic and physiological injury of Cu toxicity in kiwifruit. Cu stress assays and transcriptional analysis have shown that Cu treatment for 12 h significantly increased the AsA content in kiwifruit leaves and up-regulated key genes involved in AsA biosynthesis, such as GDP-L-galactose phosphorylase3 (GGP3) and GDP-mannose-3',5'-epimerase (GME). Overexpressing GGP3 in transgenic kiwifruit significantly increased the endogenous AsA content of kiwifruit, which was beneficial in mitigating Cu toxicity by decreasing levels of reactive oxygen species, malondialdehyde, and electrolyte leakage, as well as reducing damage to the chloroplast structure and photosystem II. This study presented a novel strategy to ameliorate plant Cu stress by increasing the endogenous antioxidant (AsA) content through transgenesis.
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Cobre , Plaguicidas , Cobre/toxicidad , Ácido Ascórbico/farmacología , Bioensayo , CloroplastosRESUMEN
Anthocyanin is a class of water-soluble flavonoids found in Chinese bayberry (Morella rubra) that is not only responsible for the variety of colors visible in nature but also has numerous health-promoting benefits in humans. Through comparative transcriptomics, we isolated and identified a transcription factor (TF) of the R2R3-MYB type, MrMYB9, in order to explore the anthocyanin biosynthesis pathway in red and white Chinese bayberries. MrMYB9 transcript was positively correlated with anthocyanin level and anthocyanin biosynthetic gene expression during Chinese bayberry fruit maturation (R-values in the range 0.54-0.84, p < 0.05). Sequence analysis revealed that MrMYB9 shared a similar R2R3 domain with MYB activators of anthocyanin biosynthesis in other plants. MrMYB9 substantially transactivated promoters of anthocyanin biosynthesis-related EBGs (MrCHI, MrF3'H, and MrANS) and LBGs (MrUFGT) upon co-expression of the AtEGL3 gene. Our findings indicated that MrMYB9 may positively modulate anthocyanin accumulation in Chinese bayberry.
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Hydrogen-rich water (HRW) treatment has been reported to delay the softening and senescence of postharvest okras, but its regulatory mechanism remains unclear. In this paper, we investigated the effects of HRW treatment on the metabolism of several phytohormones in postharvest okras, which act as regulatory molecules in fruit ripening and senescence processes. The results showed that HRW treatment delayed okra senescence and maintained fruit quality during storage. The treatment upregulated all of the melatonin biosynthetic genes such as AeTDC, AeSNAT, AeCOMT and AeT5H, contributing to the higher melatonin content in the treated okras. Meanwhile, increased transcripts of anabolic genes but lower expression of catabolic genes involved in indoleacetic acid (IAA) and gibberellin (GA) metabolism were observed in okras when treated with HRW, which was related to the enhanced levels of IAA and GA. However, the treated okras experienced lower abscisic acid (ABA) content as compared to the non-treated fruit due to the down-regulation of its biosynthetic genes and up-regulation of the degradative gene AeCYP707A. Additionally, there was no difference in γ-aminobutyric acid between the non-treated and HRW-treated okras. Collectively, our results indicated that HRW treatment increased levels of melatonin, GA and IAA, but decreased ABA content, which ultimately delayed fruit senescence and prolonged shelf life in postharvest okras.
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The effect of hydrogen-rich water (HRW) treatment on softening, cell wall components and cell wall metabolic genes in okras after harvest was studied. The results showed that HRW treatment could maintain fruit firmness and delay softening, thereby prolonging shelf life in okras during storage. The treated okras displayed significantly lower levels water- and chelate-soluble pectins while higher contents of Na2CO3-soluble pectin, hemicellulose and cellulose. The cell wall biosynthesis was maintained by HRW treatment via up-regulating genes involved in biosynthesis of pectin, hemicellulose and cellulose at the beginning of storage. On the contrary, the treatment could inhibit the cell wall disassembly due to the down-regulation of numerous cell wall degradative genes including AePME, AeGAL and AeCX at the end of storage. Taken together, our results suggested that HRW treatment delayed softening and extended shelf life in postharvest okras through modifying cell wall biosynthesis and disassembly at different times of storage.