scholarly journals Cell death in grape berries: varietal differences linked to xylem pressure and berry weight loss

2008 ◽  
Vol 35 (3) ◽  
pp. 173 ◽  
Author(s):  
Joanne Tilbrook ◽  
Stephen D. Tyerman
Keyword(s):  
Weight Loss ◽  
Cell Death ◽  
Membrane Integrity ◽  
Hydraulic Conductance ◽  
Pressure Probe ◽  
Vitis Vinifera L ◽  
Thompson Seedless ◽  
Xylem Pressure ◽  
Cell Vitality ◽  
Berry Weight

Some varieties of Vitis vinifera L. can undergo berry weight loss during later stages of ripening. This defines a third phase of development in addition to berry formation and berry expansion. Berry weight loss is due to net water loss, but the component water flows through different pathways have remained obscure. Because of the very negative osmotic potential of the cell sap, the maintenance of semipermeable membranes in the berry is required for the berry to counter xylem and apoplast tensions that may be transferred from the vine. The transfer of tension is determined by the hydraulic connection through the xylem from the berry to the vine, which changes during development. Here we assess the membrane integrity of three varieties of V. vinifera berries (cvv. Shiraz, Chardonnay and Thompson seedless) throughout development using the vitality stains, fluorescein diacetate and propidium iodide, on fresh longitudinal sections of whole berries. We also measured the xylem pressure using a pressure probe connected to the pedicel of detached berries. The wine grapes, Chardonnay and Shiraz, maintained fully vital cells after veraison and during berry expansion, but began to show cell death in the mesocarp and endocarp at or near the time that the berries attain maximum weight. This corresponded to a change in rate of accumulation of solutes in the berry and the beginning of weight loss in Shiraz, but not in Chardonnay. Continuous decline in mesocarp and endocarp cell vitality occurred for both varieties until normal harvest dates. Shiraz grapes classified as high quality and sourced from a different vineyard also showed the same death response at the same time after anthesis, but they displayed a more consistent pattern of pericarp cell death. The table grape, Thompson seedless, showed near to 100% vitality for all cells throughout development and well past normal harvest date, except for berries with noticeable berry collapse that were treated with giberellic acid. The high cell vitality in Thompson seedless berries corresponded to negative xylem pressures that contrasted to the slightly positive pressures for Shiraz and Chardonnay. We hypothesise that two variety dependent strategies exist for grapevine berries late in development: (1) programmed cell death in the pericarp and loss of osmotically competent membranes that requires concomitant reduction in the hydraulic conductance via the xylem to the vine; (2) continued cell vitality and osmotically competent membranes that can allow high hydraulic conductance to the vine.

Hydraulic connection of grape berries to the vine: varietal differences in water conductance into and out of berries, and potential for backflow

2009 ◽  
Vol 36 (6) ◽  
pp. 541 ◽  
Author(s):  
Joanne Tilbrook ◽  
Stephen D. Tyerman
Keyword(s):  
Weight Loss ◽  
Hydraulic Conductance ◽  
Pressure Probe ◽  
Vitis Vinifera L ◽  
Stem Water Potential ◽  
Thompson Seedless ◽  
Flow Rates ◽  
Hydraulic Connection ◽  
Varietal Differences ◽  
Berry Weight

Weight loss in Vitis vinifera L. cv. Shiraz berries occurs in the later stages of ripening from 90–100 days after anthesis (DAA). This rarely occurs in varieties such as Chardonnay and Thompson seedless. Flow rates of water under a constant pressure into berries on detached bunches of these varieties are similar until 90–100 DAA. Shiraz berries then maintain constant flow rates until harvest maturity, and Chardonnay inflow tapers to almost zero. Thompson seedless maintains high xylem inflows. Hydraulic conductance for flow in and out of individual Shiraz and Chardonnay berries was measured using a root pressure probe. From 105 DAA, during berry weight loss in Shiraz, there were significant varietal differences in xylem hydraulic conductance. Both varieties showed flow rectification such that conductance for inflow was higher than conductance for outflow. For flow into the berry, Chardonnay had 14% of the conductance of Shiraz. For flow out of the berry Chardonnay was 4% of the conductance of Shiraz. From conductance measurements for outflow from the berry and stem water potential measurements, it was calculated that Shiraz could loose ~7% of berry volume per day, consistent with rates of berry weight loss. A functional pathway for backflow from the berries to the vine via the xylem was visualised with Lucifer Yellow CH loaded at the cut stylar end of berries on potted vines. Transport of the dye out of the berry xylem ceased before 97 DAA in Chardonnay, but was still transported into the torus and pedicel xylem of Shiraz at 118 DAA. Xylem backflow could be responsible for a portion of the post-veraison weight loss in Shiraz berries. These data provide evidence of varietal differences in hydraulic connection of berries to the vine that we relate to cell vitality in the mesocarp. The key determinates of berry water relations appear to be maintenance or otherwise of semi permeable membranes in the mesocarp cells and control of flow to the xylem to give variable hydraulic connection back to the vine.

Quercetin in attenuation of ischemic/reperfusion injury: A review

2020 ◽  
Vol 13 ◽  
Author(s):  
Milad Ashrafizadeh ◽  
Saeed Samarghandian ◽  
Kiavash Hushmandi ◽  
Amirhossein Zabolian ◽  
Md Shahinozzaman ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Membrane ◽  
Blood Supply ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Membrane Integrity ◽  
Therapeutic Effects ◽  
Molecular Pathways ◽  
Cell Membrane Integrity ◽  
Cell Membrane Disruption

Background: Ischemia/reperfusion (I/R) injury is a serious pathologic event that occurs due to restriction in blood supply to an organ, followed by hypoxia. This condition leads to enhanced levels of pro-inflammatory cytokines such as IL-6 and TNF-, and stimulation of oxidative stress via enhancing reactive oxygen species (ROS) levels. Upon reperfusion, blood supply increases, but it deteriorates condition, and leads to generation of ROS, cell membrane disruption and finally, cell death. Plant derived-natural compounds are well-known due to their excellent antioxidant and anti-inflammatory activities. Quercetin is a flavonoid exclusively found in different vegetables, herbs, and fruits. This naturally occurring compound possesses different pharmacological activities making it appropriate option in disease therapy. Quercetin can also demonstrate therapeutic effects via affecting molecular pathways such as NF-B, PI3K/Akt and so on. Methods: In the present review, we demonstrate that quercetin administration is beneficial in ameliorating I/R injury via reducing ROS levels, inhibition of inflammation, and affecting molecular pathways such as TLR4/NF-B, MAPK and so on. Results and conclusion: Quercetin can improve cell membrane integrity via decreasing lipid peroxidation. Apoptotic cell death is inhibited by quercetin via down-regulation of Bax, and caspases, and upregulation of Bcl-2. Quercetin is able to modulate autophagy (inhibition/induction) in decreasing I/R injury. Nanoparticles have been applied for delivery of quercetin, enhancing its bioavailability and efficacy in alleviation of I/R injury. Noteworthy, clinical trials have also confirmed the capability of quercetin in reducing I/R injury.

scholarly journals Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 845
Author(s):  
Anja Sadžak ◽  
Ignacija Vlašić ◽  
Zoran Kiralj ◽  
Marijana Batarelo ◽  
Nada Oršolić ◽  
...  
Keyword(s):  
Cell Death ◽  
Intracellular Signaling ◽  
Chromatin Condensation ◽  
Membrane Integrity ◽  
Toxic Effects ◽  
Trypan Blue Exclusion ◽  
Atp Production ◽  
Mtt Method ◽  
Biophysical Approach ◽  
Induced Changes

Oxidative stress (OS) induced by the disturbed homeostasis of metal ions is one of the pivotal factors contributing to neurodegeneration. The aim of the present study was to investigate the effects of flavonoid myricetin on copper-induced toxicity in neuroblastoma SH-SY5Y cells. As determined by the MTT method, trypan blue exclusion assay and measurement of ATP production, myricetin heightened the toxic effects of copper and exacerbated cell death. It also increased copper-induced generation of reactive oxygen species, indicating the prooxidative nature of its action. Furthermore, myricetin provoked chromatin condensation and loss of membrane integrity without caspase-3 activation, suggesting the activation of both caspase-independent programmed cell death and necrosis. At the protein level, myricetin-induced upregulation of PARP-1 and decreased expression of Bcl-2, whereas copper-induced changes in the expression of p53, p73, Bax and NME1 were not further affected by myricetin. Inhibitors of ERK1/2 and JNK kinases, protein kinase A and L-type calcium channels exacerbated the toxic effects of myricetin, indicating the involvement of intracellular signaling pathways in cell death. We also employed atomic force microscopy (AFM) to evaluate the morphological and mechanical properties of SH-SY5Y cells at the nanoscale. Consistent with the cellular and molecular methods, this biophysical approach also revealed a myricetin-induced increase in cell surface roughness and reduced elasticity. Taken together, we demonstrated the adverse effects of myricetin, pointing out that caution is required when considering powerful antioxidants for adjuvant therapy in copper-related neurodegeneration.

Long-term xylem pressure measurements in the liana Tetrastigma voinierianum by means of the xylem pressure probe

Planta ◽  
1995 ◽  
Vol 196 (4) ◽  
Author(s):  
Rainer Benkert ◽  
Jian-Jun Zhu ◽  
Gertraud Zimmermann ◽  
Roman T�rk ◽  
Friedrich-Wilhelm Bentrup ◽  
...  
Keyword(s):  
Pressure Probe ◽  
Pressure Measurements ◽  
Xylem Pressure ◽  
Xylem Pressure Probe

scholarly journals Heme induces programmed necrosis on macrophages through autocrine TNF and ROS production

Blood ◽  
2012 ◽  
Vol 119 (10) ◽  
pp. 2368-2375 ◽  
Author(s):  
Guilherme B. Fortes ◽  
Leticia S. Alves ◽  
Rosane de Oliveira ◽  
Fabianno F. Dutra ◽  
Danielle Rodrigues ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Critical Role ◽  
Membrane Integrity ◽  
Iron Chelation ◽  
Heme Oxygenase 1 ◽  
Cytotoxic Effects ◽  
Interacting Protein ◽  
Free Heme ◽  
Necrosis Factor

Abstract Diseases that cause hemolysis or myonecrosis lead to the leakage of large amounts of heme proteins. Free heme has proinflammatory and cytotoxic effects. Heme induces TLR4-dependent production of tumor necrosis factor (TNF), whereas heme cytotoxicity has been attributed to its ability to intercalate into cell membranes and cause oxidative stress. We show that heme caused early macrophage death characterized by the loss of plasma membrane integrity and morphologic features resembling necrosis. Heme-induced cell death required TNFR1 and TLR4/MyD88-dependent TNF production. Addition of TNF to Tlr4−/− or to Myd88−/− macrophages restored heme-induced cell death. The use of necrostatin-1, a selective inhibitor of receptor-interacting protein 1 (RIP1, also known as RIPK1), or cells deficient in Rip1 or Rip3 revealed a critical role for RIP proteins in heme-induced cell death. Serum, antioxidants, iron chelation, or inhibition of c-Jun N-terminal kinase (JNK) ameliorated heme-induced oxidative burst and blocked macrophage cell death. Macrophages from heme oxygenase-1 deficient mice (Hmox1−/−) had increased oxidative stress and were more sensitive to heme. Taken together, these results revealed that heme induces macrophage necrosis through 2 synergistic mechanisms: TLR4/Myd88-dependent expression of TNF and TLR4-independent generation of ROS.

scholarly journals Gene-dependent yeast cell death pathway requires AP-3 vesicle trafficking leading to vacuole membrane permeabilization

2021 ◽  
Author(s):  
Zachary D Stolp ◽  
Madhura Kulkarni ◽  
Yining Liu ◽  
Chengzhang Zhu ◽  
Alizay Jalisi ◽  
...  
Keyword(s):  
Cell Death ◽  
Yeast Cell ◽  
Vesicle Trafficking ◽  
Membrane Integrity ◽  
Time Lapse ◽  
Membrane Permeabilization ◽  
Cell Death Pathway ◽  
Sequence Of Events ◽  
A Genome ◽  
Lysosome Membrane

Unicellular eukaryotes are suggested to undergo self-inflicted destruction. However, molecular details are sparse by comparison to the mechanisms of cell death known for human cells and animal models. Here we report a molecular pathway in Saccharomyces cerevisiae leading to vacuole/lysosome membrane permeabilization and cell death. Following exposure to heat-ramp conditions, a model of environmental stress, we observed that yeast cell death occurs over several hours, suggesting an ongoing molecular dying process. A genome-wide screen for death-promoting factors identified all subunits of the AP-3 adaptor complex. AP-3 promotes stress-induced cell death through its Arf1-GTPase-dependent vesicle trafficking function, which is required to transport and install proteins on the vacuole/lysosome membrane, including a death-promoting protein kinase Yck3. Time-lapse microscopy revealed a sequence of events where AP-3-dependent vacuole permeability occurs hours before the loss of plasma membrane integrity. An AP-3-dependent cell death pathway appears to be conserved in the human pathogen Cryptococcus neoformans.

scholarly journals Severe Outbreaks of Bunch Rots Caused by Rhizopus stolonifer and Aspergillus niger on Table Grapes in Chile

Plant Disease ◽  
2002 ◽  
Vol 86 (7) ◽  
pp. 815-815 ◽  
Author(s):  
B. A. Latorre ◽  
S. C. Viertel ◽  
I. Spadaro
Keyword(s):  
Aspergillus Niger ◽  
Cultural Practices ◽  
Weather Conditions ◽  
Soluble Solids ◽  
Vitis Vinifera L ◽  
Rhizopus Stolonifer ◽  
Thompson Seedless ◽  
Table Grapes ◽  
Hypodermic Syringe ◽  
Black Mold

Severe outbreaks of bunch rots (BR) have occurred recently during harvest of table grapes (Vitis vinifera L.) in Chile. Previously, BR was almost exclusively associated with Botrytis cinerea Pers.:Fr. (2,3); however, in 2000 to 2002, BR symptoms were associated with black molds and possibly nonfilamentous yeasts and bacteria. Cvs. Thompson Seedless, Flame Seedless, Ruby Seedless, and Red Globe were severely affected. Symptoms start at the pedicels as soft, watery rots that partially or completely decay infected berries. Longitudinal cracks are produced, a black mold usually develops along the crack fissures, and the skin of the berry turns light gray. Isolations on potato dextrose agar acidified with 1 N lactic acid (APDA) at 0.5 ml/liter, consistently yielded Rhizopus stolonifer (Ehrenb. ex Fr.) Vuillemin and Aspergillus niger Tiegh. R. stolonifer on APDA produced a white-to-gray aerial and nonseptate mycelium, black and globose sporangia with an elliptical collumela, one-celled, globose to oval, striated, almost hyaline sporangiospores, rhizoids, and stolons. A. niger produced septate mycelium. Single-celled, black, rough walled, globose conidia developed on short chains on the second phialides at the tip of globose, upright conidiophores. Mature (soluble solids >16%) detached berries of cv. Thompson Seedless were inoculated with sporangiospores (≈107 spores per ml) of R. stolonifer isolates RS6, RS52, RS73, and RS79 and conidia (≈108 conidia per ml) of A. niger isolates AN12, AN69, and AN75. When berries were aseptically punctured with a sterile hypodermic syringe prior to inoculation, 60 to 86.7% and 42.5 to 100% of berries were infected with R. stolonifer and A. niger, respectively, and both developed BR symptoms (significantly different from control berries) after 48 h in humid chambers at 23°C. Injuries were needed for infection since no infection or only 23.3% of noninjured berries were infected with R. stolonifer and A. niger, respectively. For both pathogens, there was a significant (P < 0.043) interaction between isolates and the presence or absence of injuries. Both pathogens were successfully reisolated on APDA. Fungicide sensitivity tests were performed on detached cv. Thompson Seedless berries challenged by placing an ≈6 μl-drop of inoculum suspension (106 or 107 spores per ml of R. stolonifer isolate RS52 and A. niger isolate AN12, respectively) on injured berries. Pyraclostrobin (0.067 mg/ml) mixed with nicobifen at 0.134 mg/ml (BAS 516 01 F at 0.201 mg a.i./ml, BASF) and copper oxide at 1.2 mg/ml (Cuprodul 60 WP, Quimetal Chile) significantly (P < 0.01) inhibited infection (100% control) by R. stolonifer and A. niger. R. stolonifer was completely controlled by dicloran at 1.88 mg/ml (Botran 75 WP) and partially controlled by captan at 1.6 mg/ml (Captan 80 WP), but A. niger was not controlled by either fungicide. To our knowledge this is the first report of R. stolonifer causing BR of table grape in Chile (4). The severe outbreaks may be associated with warm weather conditions during harvest and injuries caused by birds, insects, or cultural practices. Infection caused by R. stolonifer or A. niger may be followed by sour rot organisms (yeasts or bacteria), as has been suggested elsewhere (1,2). References: (1) E. Gravot et al. Phytoma 543:36, 2001. (2) W. B. Hewitt Page 26 in: Compendium of Grape Diseases, American Phytopathological Society, St. Paul, MN, 1994. (3) B. A. Latorre and G. Vásquez. Aconex (Chile) 52:16, 1996. (4) F. Mujica and C. Vergara. Flora Fungosa Chilena. Universidad de Chile, Facultad de Agronomiacute;a, Santiago, Chile, 1980.

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