scholarly journals Metabolic acclimation supports higher aluminium-induced secretion of citrate and malate in an aluminium-tolerant hybrid clone of Eucalyptus

2020 ◽  
Author(s):  
Wannian Li ◽  
Patrick M. Finnegan ◽  
Qin Dai ◽  
Dongqiang Guo ◽  
Mei Yang
Keyword(s):  
Organic Acid ◽  
Citrate Synthase ◽  
Time Lag ◽  
Eucalyptus Grandis ◽  
Anion Channel ◽  
Al Toxicity ◽  
Protein Synthesis Inhibitor ◽  
Al Tolerance ◽  
Synthesis Inhibitor ◽  
Citrate Secretion

Abstract Background: Eucalyptus is the main plantation wood species, mostly grown in aluminized acid soils. To understand the response of Eucalyptus clones to aluminum (Al) toxicity, the Al-tolerant Eucalyptus grandis × E. urophylla clone GL-9 (designated “G9”) and the Al-sensitive E. urophylla clone GL-4 (designated “W4”) were employed to investigate the production and secretion of citrate and malate by roots.Results: Eucalyptus seedlings in hydroponics were exposed to the presence or absence of 4.4 mM Al at pH 4.0 for 24 hours. The protein synthesis inhibitor cycloheximide (CHM) and anion channel blocker phenylglyoxal (PG) were applied to explore possible pathways involved in organic acid secretion. The secretion of malate and citrate was earlier and greater in G9 than in W4, corresponding to less Al accumulation in G9. The concentration of Al in G9 roots peaked after 1h and decreased afterwards, corresponding with a rapid induction of malate secretion. A time-lag of about 6h in citrate efflux in G9 was followed by robust secretion to support continuous Al-detoxification. Malate secretion alone may alleviate Al toxicity because the peaks of Al accumulation and malate secretion were simultaneous in W4, which did not secrete appreciable citrate. Enhanced activities of citrate synthase (CS) and phosphoenolpyruvate carboxylase (PEPC), and reduced activities of isocitrate dehydrogenase (IDH), aconitase (ACO) and malic enzyme (ME) were closely associated with the greater secretion of citrate in G9. PG effectively inhibited citrate and malate secretion in both Eucalyptus clones. CHM also inhibited malate and citrate secretion in G9, and citrate secretion in W4, but notably did not affect malate secretion in W4. Conclusions: G9 immediately secrete malate from roots, which had an initial effect on Al-detoxification, followed by time-delayed citrate secretion. Pre-existing anion channel protein first contributed to malate secretion, while synthesis of carrier protein appeared to be needed for citrate excretion. The changes of organic acid concentrations in response to Al can be achieved by enhanced CS and PEPC activities, but was supported by changes in the activities of other enzymes involved in organic acid metabolism. The above information may help to further explore genes related to Al-tolerance in Eucalyptus.

scholarly journals Metabolic acclimation supports higher aluminium-induced secretion of citrate and malate in an aluminium-tolerant hybrid clone of Eucalyptus

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Wannian Li ◽  
Patrick M. Finnegan ◽  
Qin Dai ◽  
Dongqiang Guo ◽  
Mei Yang
Keyword(s):  
Organic Acid ◽  
Citrate Synthase ◽  
Time Lag ◽  
Eucalyptus Grandis ◽  
Anion Channel ◽  
Al Toxicity ◽  
Protein Synthesis Inhibitor ◽  
Al Tolerance ◽  
Synthesis Inhibitor ◽  
Citrate Secretion

Abstract Background Eucalyptus is the main plantation wood species, mostly grown in aluminized acid soils. To understand the response of Eucalyptus clones to aluminum (Al) toxicity, the Al-tolerant Eucalyptus grandis × E. urophylla clone GL-9 (designated “G9”) and the Al-sensitive E. urophylla clone GL-4 (designated “W4”) were employed to investigate the production and secretion of citrate and malate by roots. Results Eucalyptus seedlings in hydroponics were exposed to the presence or absence of 4.4 mM Al at pH 4.0 for 24 h. The protein synthesis inhibitor cycloheximide (CHM) and anion channel blocker phenylglyoxal (PG) were applied to explore possible pathways involved in organic acid secretion. The secretion of malate and citrate was earlier and greater in G9 than in W4, corresponding to less Al accumulation in G9. The concentration of Al in G9 roots peaked after 1 h and decreased afterwards, corresponding with a rapid induction of malate secretion. A time-lag of about 6 h in citrate efflux in G9 was followed by robust secretion to support continuous Al-detoxification. Malate secretion alone may alleviate Al toxicity because the peaks of Al accumulation and malate secretion were simultaneous in W4, which did not secrete appreciable citrate. Enhanced activities of citrate synthase (CS) and phosphoenolpyruvate carboxylase (PEPC), and reduced activities of isocitrate dehydrogenase (IDH), aconitase (ACO) and malic enzyme (ME) were closely associated with the greater secretion of citrate in G9. PG effectively inhibited citrate and malate secretion in both Eucalyptus clones. CHM also inhibited malate and citrate secretion in G9, and citrate secretion in W4, but notably did not affect malate secretion in W4. Conclusions G9 immediately secrete malate from roots, which had an initial effect on Al-detoxification, followed by time-delayed citrate secretion. Pre-existing anion channel protein first contributed to malate secretion, while synthesis of carrier protein appeared to be needed for citrate excretion. The changes of organic acid concentrations in response to Al can be achieved by enhanced CS and PEPC activities, but was supported by changes in the activities of other enzymes involved in organic acid metabolism. The above information may help to further explore genes related to Al-tolerance in Eucalyptus.

scholarly journals Metabolic acclimation supports higher aluminium-induced secretion of citrate and malate in an aluminium-tolerant hybrid clone of Eucalyptus

2020 ◽  
Author(s):  
Wannian Li ◽  
Patrick Finnegan ◽  
Qin Dai ◽  
Dongqiang Guo ◽  
Mei Yang
Keyword(s):  
Organic Acid ◽  
Citrate Synthase ◽  
Time Lag ◽  
Eucalyptus Grandis ◽  
Anion Channel ◽  
Al Toxicity ◽  
Protein Synthesis Inhibitor ◽  
Al Tolerance ◽  
Synthesis Inhibitor ◽  
Citrate Secretion

Abstract Background: Eucalyptus is the main plantation wood species, mostly grown in aluminized acid soils. To understand the response of Eucalyptus clones to aluminum (Al) toxicity, the Al-tolerant Eucalyptus grandis × E. urophylla clone GL-9 (designated “G9”) and the Al-sensitive E. urophylla clone GL-4 (designated “W4”) were employed to investigate the production and secretion of citrate and malate by roots.Results: Eucalyptus seedlings in hydroponics were exposed to the presence or absence of 4.4 mM Al at pH 4.0 for 24 hours. The protein synthesis inhibitor cycloheximide (CHM) and anion channel blocker phenylglyoxal (PG) were applied to explore possible pathways involved in organic acid secretion. The secretion of malate and citrate was earlier and greater in G9 than in W4, corresponding to less Al accumulation in G9. The concentration of Al in G9 roots peaked after 1h and decreased afterwards, corresponding with a rapid induction of malate secretion. A time-lag of about 6h in citrate efflux in G9 was followed by robust secretion to support continuous Al-detoxification. Malate secretion alone may alleviate Al toxicity because the peaks of Al accumulation and malate secretion were simultaneous in W4, which did not secrete appreciable citrate. Enhanced activities of citrate synthase (CS) and phosphoenolpyruvate carboxylase (PEPC), and reduced activities of isocitrate dehydrogenase (IDH), aconitase (ACO) and malic enzyme (ME) were closely associated with the greater secretion of citrate in G9. PG effectively inhibited citrate and malate secretion in both Eucalyptus clones. CHM also inhibited malate and citrate secretion in G9, and citrate secretion in W4, but notably did not affect malate secretion in W4.Conclusions: G9 immediately secrete malate from roots, which had an initial effect on Al-detoxification, followed by time-delayed citrate secretion. Pre-existing anion channel protein first contributed to malate secretion, while synthesis of carrier protein appeared to be needed for citrate excretion. The changes of organic acid concentrations in response to Al can be achieved by enhanced CS and PEPC activities, but was supported by changes in the activities of other enzymes involved in organic acid metabolism. The above information may help to further explore genes related to Al-tolerance in Eucalyptus.

scholarly journals Metabolic acclimation supports higher aluminium-induced secretion of citrate and malate in an aluminium-tolerant hybrid clone of Eucalyptus

2020 ◽  
Author(s):  
Wannian Li ◽  
Patrick Finnegan ◽  
Qin Dai ◽  
Mei Yang
Keyword(s):  
Acid Secretion ◽  
Organic Acid ◽  
Citrate Synthase ◽  
Acid Soil ◽  
Anion Channel ◽  
Lag Phase ◽  
Protein Synthesis Inhibitor ◽  
Timber Species ◽  
Al Tolerance ◽  
Organic Acid Secretion

Abstract Background Eucalyptus is the main timber species, most of which are hybrid clones, and usually grow in aluminized acid soil in China. The exudation of organic acids from roots may contribute to detoxification of Al and lead to the Al-tolerance in Eucalyptus genotypes. To further understand the organic acid response in Al tolerance in Eucalyptus, the Al-tolerant Eucalyptus grandis × E. urophylla clone GL-9 (marked as “G9”) and the Al-sensitive Eucalyptus urophylla clone GL-4 (marked as “W4”) were used to investigate the secretion and metabolism of citrate and malate in roots. Results Eucalyptus seedlings in hydroponics were exposed to the presence or absence of 4.4 mM Al at pH 4.0 for 24 hours. The protein synthesis inhibitor cycloheximide (CHM) and the anion channel blocker phenylglyoxal (PG) were applied to explore possible pathways involved in organic acid secretion. The Al treatments caused higher Al accumulation in roots of both clones. The secretion of malate and citrate was greater in G9 than in W4, corresponding to the relatively higher tolerance in G9 to Al. The peak Al concentration occurred after 1 h in G9 roots and declined afterward, indicating the activation of detoxification to alleviate Al accumulation. After 6 h of Al exposure, the efflux of citrate dramatically increased in G9 after a substantial lag phase, while both peak Al accumulation in roots and peak malate secretion occurred and there was no induction of citrate secretion in W4. Enhanced activity for citrate synthase and phosphoenolpyruvate carboxylase, and reduced activity for NADP-isocitrate dehydrogenase, aconitase and NADP-malic enzyme were closely associated with the greater secretion of citrate in G9. Both PG and CHM were effective inhibitors of citrate and malate secretion in both Eucalyptus clones, except the malate secretion in W4 was not affected by CHM. Conclusions In two different Al-tolerant Eucalyptus clones, both secretion and internal accumulation of citrate and malate in roots were involved in Al detoxification. An anion channel on the plasma membrane could be an important mode of organic acid secretion. Citrate and relevant metabolizing enzymes led more important role in the response to Al in E. grandis × E. urophylla.

scholarly journals [ARTICLE PARTIAL RETRACTION] Organic acid carriers in tolerance to toxic aluminum in wheat

2018 ◽  
Vol 48 (10) ◽  
Author(s):  
Gerarda Beatriz Pinto da Silva ◽  
Camila Martini Zanella ◽  
Carla Andréa Delatorre ◽  
Márcia Soares Chaves ◽  
José Antônio Martinelli ◽  
...  
Keyword(s):  
Organic Acid ◽  
Root System ◽  
Cell Walls ◽  
Arable Land ◽  
Triticum Aestivum L ◽  
Al Toxicity ◽  
Sensitive Species ◽  
Al Tolerance ◽  
Winter Cereals ◽  
Almt1 Gene

ABSTRACT: Aluminum (Al) toxicity in plants is seen in about 15% of the soils worldwide, restraining yields in arable land. In Brazil, acidic soils limit production of wheat (Triticum aestivum L.) and other cereals. Al is toxic for most winter cereals when its concentration increases and soil pH is below 5. One of the main concerns with acidic soil is the increase in the mobility of Al3+ions. Al binds to cell walls in roots, preventing meristematic elongation in sensitive species, causing damage to the root system and results in lower yields. Al3+ forms highly stable complexes with phosphorus (P), limiting its availability to plants, as well as reducing cell division and elongation. To deal with Al toxicity, plants have developed strategies such as organic acid (OA) exudation by roots; this mechanism of detoxification has been well-characterized. OAs, in turn, chelate ions Al3, forming non-toxic compounds that do not penetrate the root system. Some genes responsible for Al tolerance in wheat have been identified, particularly TaALMT1 and TaMATE1B that transport malate and citrate OAs, respectively. In this review, we discussed the mechanisms by which Al damages roots those by which plants are protected, primarily through two genes. We also described the interaction of the ALMT1 gene with P and iron (Fe).

Corrigendum to: Mitochondrial enzymes and citrate transporter contribute to the aluminium-induced citrate secretion from soybean (Glycine max) roots

2010 ◽  
Vol 37 (5) ◽  
pp. 478 ◽  
Author(s):  
Muyun Xu ◽  
Jiangfeng You ◽  
Ningning Hou ◽  
Hongmei Zhang ◽  
Guang Chen ◽  
...  
Keyword(s):  
Glycine Max ◽  
Citrate Synthase ◽  
Transcript Level ◽  
Mitochondrial Enzymes ◽  
Al Tolerance ◽  
Citrate Transporter ◽  
Significant Difference ◽  
Soybean Roots ◽  
Citrate Secretion ◽  
Al Treatment

The concentration of soluble aluminium (Al) in the soil solution increases at low pH and the prevalence of toxic Al3+ cations represent the main factor limiting plant growth on acid soils. Citrate secretion from roots is an important Al-tolerance mechanism in many species including soybean. We isolated mitochondria from the roots of an Al-resistant soybean (Glycine max L.) cv. Jiyu 70 to investigate the relationship between citrate metabolism and Al-induced citrate secretion. Spectrophotometric assays revealed that the activities of mitochondrial malate dehydrogenase and citrate synthase increased and aconitase decreased with increasing of Al concentration (0–50 µM) and duration of Al treatment (30 µM Al, 0.5–9 h). Al-induced citrate secretion was inhibited by the citrate synthase inhibitor suramin, and enhanced by the aconitase inhibitor fluorocitric acid. Mersalyl acid, an inhibitor of a citrate carrier located in mitochondria membrane, also suppressed Al-induced citrate secretion. Transcript level of the mitochondrial citrate synthase gene increased in soybean roots exposed to Al, whereas expression of aconitase showed no significant difference. Expression of Gm-AlCT, a gene showing homology to Al-activated citrate transporters was also induced after 4 h in Al treatment. The Al-dependent changes in activity and expression of these enzymes are consistent with them supporting the sustained release of citrate from soybean roots.

Changes induced by aluminum stress in the organic acid content of maize seedlings: The crucial role of exogenous citrate in enhancing seedling growth

Biologia ◽  
2009 ◽  
Vol 64 (6) ◽  
Author(s):  
Radhouane Chaffai ◽  
Tinni Nouhou Seybou ◽  
Brahim Marzouk ◽  
Ezzedine Ferjani
Keyword(s):  
Organic Acids ◽  
Organic Acid ◽  
Acid Content ◽  
Al Toxicity ◽  
Maximal Effect ◽  
Maize Seedlings ◽  
Al Tolerance ◽  
Elevated Exposure ◽  
Organic Acid Content

AbstractWe have studied the effect of Al on growth and morphology of maize seedlings (Zea mays L.), the changes in organic acid content as well as the role of application of exogenous citrate in enhancing the Al tolerance. Al treatment induced inhibition of root growth, causing morphological symptoms of Al toxicity. Al decreased significantly the malate content in roots compared to control plants. However, the citrate and total organic acids did not show any change, indicating that one mechanism underlying plant defense may involve the maintenance a normal levels of organic acids in roots. The succinate content increased in roots at 1000 µmol L−1 Al, while that of lactate decreased. However, 500 and 1000 µmol L−1 Al significantly increased the total organic acid in shoots, due to an increase in the succinate and malate contents. By contrast, the citrate and lactate levels decreased at 250 and 500 µmol L−1 Al. To investigate the role of citrate in enhancing the plant growth, citrate was supplied to nutrient medium containing 500 µmol L−1 Al at different Al:Citrate ratios (1:1, 1:2 and 1:3). The addition of citrate in the nutrient solution resulted in an alleviation of Al toxicity, with the maximal effect obtained at Al:Citrate ratio of 1:2. These data provide evidence that in maize, the organic acids, mainly citrate play an important role in enabling the plant to tolerate elevated exposure to Al concentration.

Mitochondrial enzymes and citrate transporter contribute to the aluminium-induced citrate secretion from soybean (Glycine max) roots

2010 ◽  
Vol 37 (4) ◽  
pp. 285 ◽  
Author(s):  
Muyun Xu ◽  
Jiangfeng You ◽  
Ningning Hou ◽  
Hongmei Zhang ◽  
Guang Chen ◽  
...  
Keyword(s):  
Glycine Max ◽  
Citrate Synthase ◽  
Transcript Level ◽  
Mitochondrial Enzymes ◽  
Al Tolerance ◽  
Citrate Transporter ◽  
Significant Difference ◽  
Soybean Roots ◽  
Citrate Secretion ◽  
Al Treatment

The concentration of soluble aluminium (Al) in the soil solution increases at low pH and the prevalence of toxic Al3+ cations represent the main factor limiting plant growth on acid soils. Citrate secretion from roots is an important Al-tolerance mechanism in many species including soybean. We isolated mitochondria from the roots of an Al-resistant soybean (Glycine max L.) cv. Jiyu 70 to investigate the relationship between citrate metabolism and Al-induced citrate secretion. Spectrophotometric assays revealed that the activities of mitochondrial malate dehydrogenase and citrate synthase increased and aconitase decreased with increasing of Al concentration (0–50 µM) and duration of Al treatment (30 µM Al, 0.5–9 h). Al-induced citrate secretion was inhibited by the citrate synthase inhibitor suramin, and enhanced by the aconitase inhibitor fluorocitric acid. Mersalyl acid, an inhibitor of a citrate carrier located in mitochondria membrane, also suppressed Al-induced citrate secretion. Transcript level of the mitochondrial citrate synthase gene increased in soybean roots exposed to Al, whereas expression of aconitase showed no significant difference. Expression of Gm-AlCT, a gene showing homology to Al-activated citrate transporters was also induced after 4 h in Al treatment. The Al-dependent changes in activity and expression of these enzymes are consistent with them supporting the sustained release of citrate from soybean roots.

Mechanisms of regulation of G11α protein by dexamethasone in osteoblastic UMR 106–01 cells

2002 ◽  
Vol 282 (1) ◽  
pp. E24-E30 ◽  
Author(s):  
Ricky Cheung ◽  
Jane Mitchell
Keyword(s):  
De Novo ◽  
Mrna Level ◽  
Time Lag ◽  
Regulatory Protein ◽  
Protein Synthesis Inhibitor ◽  
Osteosarcoma Cell ◽  
Dependent Manner ◽  
Synthesis Inhibitor ◽  
Glucocorticoid Treatment ◽  
Umr 106

We have previously demonstrated that glucocorticoids increased Gq/11α protein expression and phospholipase C activity in the rat osteosarcoma cell line UMR 106–01. In this study, we demonstrated that G11α is the primary Gq-subtype family member expressed in UMR cells. Dexamethasone treatment increased the expression of G11α protein in both a time- and a dose-dependent manner. Glucocorticoid treatment significantly increased the half-life of G11α protein from 20.3 to 63 h. Steady-state G11α mRNA level was also increased by glucocorticoid treatment by ∼70%. This change was not the result of changes in RNA stability but rather the result of increased transcription, because the glucocorticoid-mediated upregulation of G11α mRNA was blocked by the transcription inhibitor actinomycin D. The dexamethasone induction of G11α mRNA occurred after a time lag of 12–24 h and was blocked by the protein synthesis inhibitor cycloheximide. These results suggest that the dexamethasone-induced rise in G11α protein results primarily from changes in the degradation rate of the protein, whereas changes in G11α mRNA play a smaller role and require de novo synthesis of regulatory protein(s).

Modulation of Arachidonic Acid Metabolism in Human Endothelial Cells by Glucocorticoids

1986 ◽  
Vol 55 (03) ◽  
pp. 369-374 ◽  
Author(s):  
Raffaele De Caterina ◽  
Babette B Weksler
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Arachidonic Acid Metabolism ◽  
Protein Synthesis Inhibitor ◽  
Synthesis Inhibitor ◽  
Prolonged Incubation ◽  
Dependent Inhibition ◽  
Human Thrombin ◽  
Umbilical Vein Endothelial Cells

SummaryTo learn whether glucocorticoids inhibit prostaglandin (PG) production in vascular endothelial cells, we investigated the effects of glucocorticoids on PG synthesis by cultured human umbilical vein endothelial cells (EC). Pretreatment of EC with dexamethasone (DX, 10-9 to 5 x 10-5 M) caused a dose-dependent inhibition of PGI2 production when PG synthesis from endogenous arachidonate was stimulated by human thrombin (0.25-2 U/ml) or ionophore A 23187 (1-5 μM). The inhibition was detectable at 10-7 M DX and maximal at 10-5 M (4.0 ± 0.7 vs. control: 7.7 ± 1.9 ng/ml, mean ± S.D., P <0.01). The production of PGE2 and the release of radiolabelled arachidonate (AA) from prelabelled cells were similarly inhibited. Prolonged incubation of EC with glucocorticoids was required to inhibit PG production or arachidonate release: ranging from 8% inhibition at 5 h to 44% at 38 h. In contrast, prostaglandin formation from exogenous AA was not altered by DX treatment. When thrombin or ionophore-stimulated EC were restimulated with exogenous AA (25 μM), DX-treated cells released more PGI2 than control cells (5.7 ± 0.5 vs. 4.1 ± 0.6 ng/ml, P <0.01). Both the decrease in PGI2 production after thrombin/ionophore and the increase after re-stimulation with AA were blunted in the presence of the protein synthesis inhibitor cycloheximide (0.1-0.2 μg/ml). Thus, incubation of EC with glucocorticoids inhibits PG production at the step of phospholipase activation. The time requirement for these steroid effects and their blunting by cycloheximide are consistent with the induction of regulatory proteins, possibly lipocortins, in endothelial cells.

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