Search claims · PlantClaims

Inactivation of Carbonyl-Detoxifying Enzymes by H2O2 Is a Trigger to Increase Carbonyl Load for Initiating Programmed Cell Death in Plants 8

Intervention effectobservedoriginal resultmeasured

Claim · model-written summary

The proteasome inhibitor MG132 suppressed H2O2-induced PCD in BY-2 cells.

Taxon: tobacco Bright Yellow-2 (BY-2) cellse0
Treatment: proteasome inhibitor MG132e4
Outcome: H2O2-induced PCDe4
Direction: suppressede4

Not reportedComparator

Verbatim

e0
“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
✓ located verbatim in the source · abstract, characters 0–80

e4
“The proteasome inhibitor MG132 suppressed the H2O2-induced PCD”
✓ located verbatim in the source · abstract, characters 864–926

Title

Inactivation of Carbonyl-Detoxifying Enzymes by H2O2 Is a Trigger to Increase Carbonyl Load for Initiating Programmed Cell Death in Plants

Md. Sanaullah Biswas; Ryota Terada; Jun’ichi Mano Antioxidants 2020. doi:10.3390/antiox9020141

Other claims from this paper (7)

Mechanismauthor interpretationoriginal resultmeasured

Claim · model-written summary

The authors propose that H2O2 inactivates a carbonyl reductase, letting RCS rise and activating C3LP activity of the 20S proteasome, which triggers PCD.

Taxon: tobacco Bright Yellow-2 (BY-2) cellse0
Gene: carbonyl reductase(s)e7
Outcome: PCD-triggering mechanisme7
Qualifier: H2O2 first inactivates a carbonyl reductase(s), allowing RCS levels to risee7

Verbatim

e0
“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
✓ located verbatim in the source · abstract, characters 0–80

e7
“Taken together, these results suggest a PCD-triggering mechanism in which H2O2 first inactivates a carbonyl reductase(s), allowing RCS levels to rise, and eventually leads to the activation of the C3LP activity of 20S proteasome”
✓ located verbatim in the source · abstract, characters 1113–1341

Title

Inactivation of Carbonyl-Detoxifying Enzymes by H2O2 Is a Trigger to Increase Carbonyl Load for Initiating Programmed Cell Death in Plants

Md. Sanaullah Biswas; Ryota Terada; Jun’ichi Mano Antioxidants 2020. doi:10.3390/antiox9020141

Other claims from this paper (7)

Intervention effect The C3LP activity increased twofold after a lethal dose of H2O2 but not after a sublethal dose in BY-2 cells.
Intervention effect Intracellular RCS levels (4-hydroxy-(E)-hexenal and HNE) increased 1.2–1.5-fold after a lethal dose of H2O2 in BY-2 cells.
Intervention effect NADPH-dependent carbonyl reductase activity decreased after a lethal dose of H2O2 in BY-2 cells.
Intervention effect The proteasome inhibitor MG132 suppressed H2O2-induced PCD in BY-2 cells.
Mechanism The C3LP activity of the beta1 subunit of the 20S proteasome is responsible for PCD in BY-2 cells.
Intervention effect H2O2 added to cell-free protein extract inactivated the carbonyl reductase.
Mechanism The carbonyl reductase acts as an ROS sensor for triggering PCD in BY-2 cells.

Mechanismauthor interpretationoriginal resultmeasured

Claim · model-written summary

The carbonyl reductase acts as an ROS sensor for triggering PCD in BY-2 cells.

Taxon: tobacco Bright Yellow-2 (BY-2) cellse0
Gene: carbonyl reductasee2
Outcome: PCDe2

Verbatim

e0
“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
✓ located verbatim in the source · abstract, characters 0–80

e2
“The carbonyl reductase thus acts as an ROS sensor for triggering PCD”
✓ located verbatim in the source · abstract, characters 1343–1411

Title

Inactivation of Carbonyl-Detoxifying Enzymes by H2O2 Is a Trigger to Increase Carbonyl Load for Initiating Programmed Cell Death in Plants

Md. Sanaullah Biswas; Ryota Terada; Jun’ichi Mano Antioxidants 2020. doi:10.3390/antiox9020141

Other claims from this paper (7)

Spermidine Exodus and Oxidation in the Apoplast Induced by Abiotic Stress Is Responsible for H2O2 Signatures That Direct Tolerance Responses in Tobacco 7

Show all 7 →

Associationobservedoriginal resultmeasured

Claim · model-written summary

Induction of stress-responsive genes or PCD depended on the level of spermidine-derived apoplastic H2O2.

Taxon: tobaccoNicotiana tabacume0
Compound: Spd-derived apoplastic H2O2e6
Outcome: Induction of either stress-responsive genes or PCDe6

Not reportedDirection

Verbatim

e0
“we developed a series of tobacco (Nicotiana tabacum cv Xanthi) transgenic plants overexpressing or downregulating apoplastic polyamine oxidase (PAO; S-pao and A-pao plants, respectively) or downregulating S-adenosyl-l-methionine decarboxylase (samdc plants)”
✓ located verbatim in the source · abstract, characters 234–491

e6
“Induction of either stress-responsive genes or PCD was dependent on the level of Spd-derived apoplastic H2O2”
✓ located verbatim in the source · abstract, characters 790–898

Title

Spermidine Exodus and Oxidation in the Apoplast Induced by Abiotic Stress Is Responsible for H2O2 Signatures That Direct Tolerance Responses in Tobacco

Panagiotis N. Moschou; Konstantinos A. Paschalidis; Ioannis D. Delis; et al. The Plant Cell 2008. doi:10.1105/tpc.108.059733

Other claims from this paper (9)

Intervention effect A-pao tobacco plants accumulated less H2O2 than wild-type plants under salt stress.
Intervention effect A-pao tobacco plants showed less programmed cell death than wild-type plants under salt stress.
Intervention effect S-pao tobacco plants had higher H2O2 levels under salt stress.
Intervention effect S-pao tobacco plants failed to accumulate stress-responsive mRNAs under salt stress.
Intervention effect Stress-responsive genes were efficiently induced in wild-type and A-pao plants, at a lower rate in A-pao plants.
Intervention effect Decreasing intracellular polyamines in samdc downregulating plants enhanced salinity-induced PCD.
Observation Tobacco plants secreted spermidine into the apoplast under salt stress.
Mechanism Apoplastic spermidine oxidized by the apoplastic PAO generates H2O2.
Mechanism Accumulated H2O2 induces tolerance responses or PCD, depending also on intracellular polyamine levels.

Mechanismauthor interpretationoriginal resultmeasured

Claim · model-written summary

Accumulated H2O2 induces tolerance responses or PCD, depending also on intracellular polyamine levels.

Taxon: tobaccoNicotiana tabacume0
Compound: H2O2e7
Outcome: induction of either tolerance responses or PCDe7
Qualifier: depending also on the levels of intracellular PAse7

Verbatim

e0
“we developed a series of tobacco (Nicotiana tabacum cv Xanthi) transgenic plants overexpressing or downregulating apoplastic polyamine oxidase (PAO; S-pao and A-pao plants, respectively) or downregulating S-adenosyl-l-methionine decarboxylase (samdc plants)”
✓ located verbatim in the source · abstract, characters 234–491

e7
“The accumulated H2O2 results in the induction of either tolerance responses or PCD, depending also on the levels of intracellular PAs”
✓ located verbatim in the source · abstract, characters 1442–1575

Title

Spermidine Exodus and Oxidation in the Apoplast Induced by Abiotic Stress Is Responsible for H2O2 Signatures That Direct Tolerance Responses in Tobacco

Panagiotis N. Moschou; Konstantinos A. Paschalidis; Ioannis D. Delis; et al. The Plant Cell 2008. doi:10.1105/tpc.108.059733

Other claims from this paper (9)

Intervention effect A-pao tobacco plants accumulated less H2O2 than wild-type plants under salt stress.
Intervention effect A-pao tobacco plants showed less programmed cell death than wild-type plants under salt stress.
Intervention effect S-pao tobacco plants had higher H2O2 levels under salt stress.
Intervention effect S-pao tobacco plants failed to accumulate stress-responsive mRNAs under salt stress.
Intervention effect Stress-responsive genes were efficiently induced in wild-type and A-pao plants, at a lower rate in A-pao plants.
Intervention effect Decreasing intracellular polyamines in samdc downregulating plants enhanced salinity-induced PCD.
Observation Tobacco plants secreted spermidine into the apoplast under salt stress.
Mechanism Apoplastic spermidine oxidized by the apoplastic PAO generates H2O2.
Association Induction of stress-responsive genes or PCD depended on the level of spermidine-derived apoplastic H2O2.

Intervention effectobservedoriginal resultmeasured

Claim · model-written summary

Decreasing intracellular polyamines in samdc downregulating plants enhanced salinity-induced PCD.

Taxon: tobaccoNicotiana tabacume0
Material: samdc downregulating transgenic plantse5
Treatment: decreasing intracellular PAse5
Outcome: salinity-induced PCDe5
Direction: enhancede5

Not reportedComparator

Verbatim

e0
“we developed a series of tobacco (Nicotiana tabacum cv Xanthi) transgenic plants overexpressing or downregulating apoplastic polyamine oxidase (PAO; S-pao and A-pao plants, respectively) or downregulating S-adenosyl-l-methionine decarboxylase (samdc plants)”
✓ located verbatim in the source · abstract, characters 234–491

e5
“decreasing intracellular PAs, while keeping normal apoplastic Spd oxidation, as in samdc downregulating transgenic plants, caused enhanced salinity-induced PCD”
✓ located verbatim in the source · abstract, characters 1153–1312

Title

Spermidine Exodus and Oxidation in the Apoplast Induced by Abiotic Stress Is Responsible for H2O2 Signatures That Direct Tolerance Responses in Tobacco

Panagiotis N. Moschou; Konstantinos A. Paschalidis; Ioannis D. Delis; et al. The Plant Cell 2008. doi:10.1105/tpc.108.059733

Other claims from this paper (9)

Intervention effect A-pao tobacco plants accumulated less H2O2 than wild-type plants under salt stress.
Intervention effect A-pao tobacco plants showed less programmed cell death than wild-type plants under salt stress.
Intervention effect S-pao tobacco plants had higher H2O2 levels under salt stress.
Intervention effect S-pao tobacco plants failed to accumulate stress-responsive mRNAs under salt stress.
Intervention effect Stress-responsive genes were efficiently induced in wild-type and A-pao plants, at a lower rate in A-pao plants.
Observation Tobacco plants secreted spermidine into the apoplast under salt stress.
Mechanism Apoplastic spermidine oxidized by the apoplastic PAO generates H2O2.
Association Induction of stress-responsive genes or PCD depended on the level of spermidine-derived apoplastic H2O2.
Mechanism Accumulated H2O2 induces tolerance responses or PCD, depending also on intracellular polyamine levels.

Cobalt Alleviates GA-Induced Programmed Cell Death in Wheat Aleurone Layers via the Regulation of H2O2 Production and Heme Oxygenase-1 Expression 6

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Mechanismobservedoriginal resultmeasured

Claim · model-written summary

Cobalt-induced initial H2O2 production may alleviate cell death.

Taxon: WheatTriticum aestivumt0
Compound: H2O2e0
Outcome: alleviation of PCDe0

Verbatim

e0
“The stimulation of HO-1 expression, and alleviation of PCD might be caused by the initial H2O2 production induced by cobalt.”
✓ located verbatim in the source · abstract, characters 706–830

t0
“Wheat”
✓ located verbatim in the source · title, characters 54–59

Title

Cobalt Alleviates GA-Induced Programmed Cell Death in Wheat Aleurone Layers via the Regulation of H2O2 Production and Heme Oxygenase-1 Expression

Mingzhu Wu; Jiale Li; Fangquan Wang; et al. International Journal of Molecular Sciences 2014. doi:10.3390/ijms151121155

Other claims from this paper (9)

Intervention effect Cobalt delayed GA-induced programmed cell death in wheat aleurone layers.
Intervention effect Carbon monoxide pretreatment produced a similar delay of cell death.
Intervention effect Bilirubin pretreatment produced a similar delay of cell death.
Mechanism Increased HO-1 expression contributed to cobalt alleviation of cell death.
Intervention effect ZnPPIX substantially prevented cobalt-induced increases in HO-1 activity.
Intervention effect ZnPPIX substantially prevented cobalt-induced alleviation of cell death.
Mechanism Cobalt-induced initial H2O2 production may stimulate HO-1 expression.
Observation Cobalt-induced SOD, CAT and APX expression and activities were consistent with H2O2 accumulation during GA treatment.
Intervention effect ZnPPIX differentially blocked cobalt responses.

Mechanismobservedoriginal resultmeasured

Claim · model-written summary

Cobalt-induced initial H2O2 production may stimulate HO-1 expression.

Taxon: WheatTriticum aestivumt0
Gene: HO-1e0
Compound: H2O2e0
Outcome: stimulation of HO-1 expressione0

Verbatim

e0
“The stimulation of HO-1 expression, and alleviation of PCD might be caused by the initial H2O2 production induced by cobalt.”
✓ located verbatim in the source · abstract, characters 706–830

t0
“Wheat”
✓ located verbatim in the source · title, characters 54–59

Title

Cobalt Alleviates GA-Induced Programmed Cell Death in Wheat Aleurone Layers via the Regulation of H2O2 Production and Heme Oxygenase-1 Expression

Mingzhu Wu; Jiale Li; Fangquan Wang; et al. International Journal of Molecular Sciences 2014. doi:10.3390/ijms151121155

Other claims from this paper (9)

Intervention effect Cobalt delayed GA-induced programmed cell death in wheat aleurone layers.
Intervention effect Carbon monoxide pretreatment produced a similar delay of cell death.
Intervention effect Bilirubin pretreatment produced a similar delay of cell death.
Mechanism Increased HO-1 expression contributed to cobalt alleviation of cell death.
Intervention effect ZnPPIX substantially prevented cobalt-induced increases in HO-1 activity.
Intervention effect ZnPPIX substantially prevented cobalt-induced alleviation of cell death.
Mechanism Cobalt-induced initial H2O2 production may alleviate cell death.
Observation Cobalt-induced SOD, CAT and APX expression and activities were consistent with H2O2 accumulation during GA treatment.
Intervention effect ZnPPIX differentially blocked cobalt responses.

Intervention effectobservedoriginal resultmeasured

Claim · model-written summary

Cobalt delayed GA-induced programmed cell death in wheat aleurone layers.

Taxon: wheatTriticum aestivume0
Organ / stage: aleurone layerse0
Treatment: cobalte0
Outcome: programmed cell death (PCD)e0
Direction: delaye0

Not reportedComparator

Verbatim

e0
“cobalt is able to delay gibberellic acid (GA)-induced programmed cell death (PCD) in wheat aleurone layers”
✓ located verbatim in the source · abstract, characters 171–277

Title

Cobalt Alleviates GA-Induced Programmed Cell Death in Wheat Aleurone Layers via the Regulation of H2O2 Production and Heme Oxygenase-1 Expression

Mingzhu Wu; Jiale Li; Fangquan Wang; et al. International Journal of Molecular Sciences 2014. doi:10.3390/ijms151121155

Other claims from this paper (9)

Intervention effect Carbon monoxide pretreatment produced a similar delay of cell death.
Intervention effect Bilirubin pretreatment produced a similar delay of cell death.
Mechanism Increased HO-1 expression contributed to cobalt alleviation of cell death.
Intervention effect ZnPPIX substantially prevented cobalt-induced increases in HO-1 activity.
Intervention effect ZnPPIX substantially prevented cobalt-induced alleviation of cell death.
Mechanism Cobalt-induced initial H2O2 production may stimulate HO-1 expression.
Mechanism Cobalt-induced initial H2O2 production may alleviate cell death.
Observation Cobalt-induced SOD, CAT and APX expression and activities were consistent with H2O2 accumulation during GA treatment.
Intervention effect ZnPPIX differentially blocked cobalt responses.

The soluble proteome of tobacco Bright Yellow-2 cells undergoing H2O2-induced programmed cell death 6

Show all 6 →

Observationobservedoriginal resultnegativemeasured

Claim · model-written summary

Anti-PCD signalling cascades were inhibited during peroxide-induced programmed cell death.

Taxon: tobaccoNicotiana tabacumt0
Outcome: anti-PCD signalling cascadese0
Direction: inhibitede0

Verbatim

e0
“The antioxidant defence system and the anti-PCD signalling cascades are inhibited.”
✓ located verbatim in the source · abstract, characters 872–954

t0
“tobacco Bright Yellow-2 cells”
✓ located verbatim in the source · title, characters 24–53

Title

The soluble proteome of tobacco Bright Yellow-2 cells undergoing H2O2-induced programmed cell death

C. Vannini; M. Marsoni; C. Cantara; et al. Journal of Experimental Botany 2012. doi:10.1093/jxb/ers031

Other claims from this paper (8)

Intervention effectobservedoriginal resultnegativemeasured

Claim · model-written summary

Hydrogen peroxide induced programmed cell death in tobacco Bright Yellow-2 cultures.

Taxon: tobaccoNicotiana tabacume0
Material: Bright Yellow-2 (TBY-2)e0
Treatment: 50 mM H₂O₂e0
Outcome: PCDe0

Not reportedComparatorDirection

Verbatim

e0
“The addition of 50 mM H₂O₂ to tobacco Bright Yellow-2 (TBY-2) cell cultures induces PCD.”
✓ located verbatim in the source · abstract, characters 191–279

Title

The soluble proteome of tobacco Bright Yellow-2 cells undergoing H2O2-induced programmed cell death

C. Vannini; M. Marsoni; C. Cantara; et al. Journal of Experimental Botany 2012. doi:10.1093/jxb/ers031

Other claims from this paper (8)

Observationobservedoriginal resultnegativemeasured

Claim · model-written summary

Tobacco cells undergoing peroxide-induced programmed cell death failed to cope with oxidative stress.

Taxon: tobaccoNicotiana tabacumt0
Outcome: fail to cope with oxidative stresse0

Verbatim

e0
“Cells undergoing H₂O₂-induced PCD fail to cope with oxidative stress.”
✓ located verbatim in the source · abstract, characters 802–871

t0
“tobacco Bright Yellow-2 cells”
✓ located verbatim in the source · title, characters 24–53

Title

The soluble proteome of tobacco Bright Yellow-2 cells undergoing H2O2-induced programmed cell death

C. Vannini; M. Marsoni; C. Cantara; et al. Journal of Experimental Botany 2012. doi:10.1093/jxb/ers031

Other claims from this paper (8)

Intervention effect Hydrogen peroxide induced programmed cell death in tobacco Bright Yellow-2 cultures.
Intervention effect Hydrogen peroxide treatment caused early down-regulation of several redox hub elements.
Intervention effect Hydrogen peroxide treatment inhibited the protein repair-degradation system.
Observation Homeostatic response protein expression patterns, particularly metabolism-related proteins, were altered.
Observation Cytoskeleton protein abundance changed during programmed cell death.
Observation The antioxidant defence system was inhibited during peroxide-induced programmed cell death.
Observation Anti-PCD signalling cascades were inhibited during peroxide-induced programmed cell death.
Observation Fifteen proteins had differential expression resembling the pattern previously seen in heat shock induced cell death.

Involvement of the mitochondrial KATP+ channel in H2O2- or NO-induced programmed death of soybean suspension cell cultures 4

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Mechanismauthor interpretationoriginal resultmeasured

Claim · model-written summary

The authors implicate a K(+)ATP channel in H2O2- or NO-induced programmed cell death.

Taxon: soybeanGlycine maxt0
Gene: K(+)ATP channele0
Outcome: PCDe0

Verbatim

e0
“These results point to the involvement of a K(+)ATP channel during the manifestation of PCD induced by H2O2 or NO in plants.”
✓ located verbatim in the source · abstract, characters 1691–1815

t0
“soybean suspension cell cultures”
✓ located verbatim in the source · title, characters 90–122

Title

Involvement of the mitochondrial KATP+ channel in H2O2- or NO-induced programmed death of soybean suspension cell cultures

V. Casolo Journal of Experimental Botany 2005. doi:10.1093/jxb/eri093

Other claims from this paper (16)

Intervention effect Hydrogen peroxide at 5 mM induced programmed cell death.
Intervention effect Cells treated with 20 mM H2O2 became necrotic, with intermediate necrapoptotic hallmarks before that.
Observation ATP and glucose-6-phosphate stayed constant during programmed cell death.
Observation ATP and glucose-6-phosphate decreased significantly in necrotic cells.
Intervention effect Succinate-dependent oxygen consumption was slightly uncoupled in mitochondria from 5 mM H2O2-treated cells.
Intervention effect Mitochondrial electrical potential difference weakly decreased after 5 mM H2O2 treatment.
Intervention effect KCl caused greater partial dissipation of delta psi in treated mitochondria than in controls.
Mechanism CsA induced delta psi formation in de-energized mitochondria through K+ efflux.
Intervention effect CsA-induced K+ efflux was reduced in mitochondria from treated cells.
Observation Mitochondria from 1 mM sodium nitroprusside-treated cells showed the same response pattern and apoptotic symptoms.
Intervention effect Succinate-dependent oxygen consumption was completely uncoupled in necrotic cells treated with 20 mM H2O2.
Intervention effect Delta psi generation was significantly inhibited in necrotic cells treated with 20 mM H2O2.
Intervention effect CsA-dependent delta psi formation was prevented in necrotic cells treated with 20 mM H2O2.
Intervention effect Mitochondrial swelling was partly prevented in apoptotic cells compared with control cells.
Intervention effect Mitochondrial swelling was completely prevented in necrotic cells compared with control cells.
Observation Moderate swelling accompanied slight outer-membrane rupture and cytochrome c release.

Intervention effectobservedoriginal resultnegativemeasured

Claim · model-written summary

Hydrogen peroxide at 5 mM induced programmed cell death.

Taxon: soybeanGlycine maxt0
Treatment: Hydrogen peroxide (5 mM)e0
Outcome: PCDe0

Not reportedComparatorDirection

Verbatim

e0
“Hydrogen peroxide (5 mM) induced PCD.”
✓ located verbatim in the source · abstract, characters 140–177

t0
“soybean suspension cell cultures”
✓ located verbatim in the source · title, characters 90–122

Title

Involvement of the mitochondrial KATP+ channel in H2O2- or NO-induced programmed death of soybean suspension cell cultures

V. Casolo Journal of Experimental Botany 2005. doi:10.1093/jxb/eri093

Other claims from this paper (16)

Intervention effect Cells treated with 20 mM H2O2 became necrotic, with intermediate necrapoptotic hallmarks before that.
Observation ATP and glucose-6-phosphate stayed constant during programmed cell death.
Observation ATP and glucose-6-phosphate decreased significantly in necrotic cells.
Intervention effect Succinate-dependent oxygen consumption was slightly uncoupled in mitochondria from 5 mM H2O2-treated cells.
Intervention effect Mitochondrial electrical potential difference weakly decreased after 5 mM H2O2 treatment.
Intervention effect KCl caused greater partial dissipation of delta psi in treated mitochondria than in controls.
Mechanism CsA induced delta psi formation in de-energized mitochondria through K+ efflux.
Intervention effect CsA-induced K+ efflux was reduced in mitochondria from treated cells.
Observation Mitochondria from 1 mM sodium nitroprusside-treated cells showed the same response pattern and apoptotic symptoms.
Intervention effect Succinate-dependent oxygen consumption was completely uncoupled in necrotic cells treated with 20 mM H2O2.
Intervention effect Delta psi generation was significantly inhibited in necrotic cells treated with 20 mM H2O2.
Intervention effect CsA-dependent delta psi formation was prevented in necrotic cells treated with 20 mM H2O2.
Intervention effect Mitochondrial swelling was partly prevented in apoptotic cells compared with control cells.
Intervention effect Mitochondrial swelling was completely prevented in necrotic cells compared with control cells.
Observation Moderate swelling accompanied slight outer-membrane rupture and cytochrome c release.
Mechanism The authors implicate a K(+)ATP channel in H2O2- or NO-induced programmed cell death.

Observationobservedoriginal resultmeasured

Claim · model-written summary

ATP and glucose-6-phosphate stayed constant during programmed cell death.

Taxon: soybeanGlycine maxt0
Outcome: The level of ATP and of glucose-6-phosphatee0
Direction: remained constante0
Qualifier: cells undergoing PCDe0

Verbatim

e0
“The level of ATP and of glucose-6-phosphate remained constant in cells undergoing PCD”
✓ located verbatim in the source · abstract, characters 295–380

t0
“soybean suspension cell cultures”
✓ located verbatim in the source · title, characters 90–122

Title

Involvement of the mitochondrial KATP+ channel in H2O2- or NO-induced programmed death of soybean suspension cell cultures

V. Casolo Journal of Experimental Botany 2005. doi:10.1093/jxb/eri093

Other claims from this paper (16)

Intervention effect Hydrogen peroxide at 5 mM induced programmed cell death.
Intervention effect Cells treated with 20 mM H2O2 became necrotic, with intermediate necrapoptotic hallmarks before that.
Observation ATP and glucose-6-phosphate decreased significantly in necrotic cells.
Intervention effect Succinate-dependent oxygen consumption was slightly uncoupled in mitochondria from 5 mM H2O2-treated cells.
Intervention effect Mitochondrial electrical potential difference weakly decreased after 5 mM H2O2 treatment.
Intervention effect KCl caused greater partial dissipation of delta psi in treated mitochondria than in controls.
Mechanism CsA induced delta psi formation in de-energized mitochondria through K+ efflux.
Intervention effect CsA-induced K+ efflux was reduced in mitochondria from treated cells.
Observation Mitochondria from 1 mM sodium nitroprusside-treated cells showed the same response pattern and apoptotic symptoms.
Intervention effect Succinate-dependent oxygen consumption was completely uncoupled in necrotic cells treated with 20 mM H2O2.
Intervention effect Delta psi generation was significantly inhibited in necrotic cells treated with 20 mM H2O2.
Intervention effect CsA-dependent delta psi formation was prevented in necrotic cells treated with 20 mM H2O2.
Intervention effect Mitochondrial swelling was partly prevented in apoptotic cells compared with control cells.
Intervention effect Mitochondrial swelling was completely prevented in necrotic cells compared with control cells.
Observation Moderate swelling accompanied slight outer-membrane rupture and cytochrome c release.
Mechanism The authors implicate a K(+)ATP channel in H2O2- or NO-induced programmed cell death.

Post-Transcriptional Suppression of Cytosolic Ascorbate Peroxidase Expression during Pathogen-Induced Programmed Cell Death in Tobacco 2

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Mechanismauthor interpretationoriginal resultmeasured

Claim · model-written summary

The authors infer cAPX suppression reduces H2O2 scavenging and enables H2O2 accumulation and faster PCD.

Taxon: TobaccoNicotiana tabacumt0
Compound: H2O2e0
Outcome: acceleration of PCDe0
Direction: acceleratione0
Qualifier: reduction in the capability of cells to scavenge H2O2e0

Verbatim

e0
“This suppression is likely to contribute to a reduction in the capability of cells to scavenge H2O2, which in turn enables the accumulation of H2O2 and the acceleration of PCD”
✓ located verbatim in the source · abstract, characters 1228–1403

t0
“Tobacco”
✓ located verbatim in the source · title, characters 127–134

Title

Post-Transcriptional Suppression of Cytosolic Ascorbate Peroxidase Expression during Pathogen-Induced Programmed Cell Death in Tobacco

Ron Mittler; Xuqiao Feng; Mira Cohen The Plant Cell 1998. doi:10.1105/tpc.10.3.461

Other claims from this paper (7)

Observation During viral induced PCD in tobacco, cAPX expression was suppressed after transcription.
Observation cAPX transcripts increased during PCD.
Observation cAPX protein levels declined during PCD.
Observation In vivo labeling and immunoprecipitation indicated inhibited cAPX protein synthesis.
Observation cAPX transcripts remained associated with polysomes during PCD.
Observation No cAPX protein was detected after in vitro polysome run off assays.
Mechanism The authors suggest cAPX suppression may occur at translation elongation.

Observationobservedoriginal resultnegativemeasured

Claim · model-written summary

During viral induced PCD in tobacco, cAPX expression was suppressed after transcription.

Taxon: tobaccoNicotiana tabacume0
Gene: cytosolic ascorbate peroxidase (cAPX)e0
Outcome: expression of cytosolic ascorbate peroxidase (cAPX)e0
Direction: suppressede0
Qualifier: viral-induced PCDe0

Verbatim

e0
“during viral-induced PCD in tobacco, the expression of cytosolic ascorbate peroxidase (cAPX), a key H2O2 detoxifying enzyme, is post-transcriptionally suppressed”
✓ located verbatim in the source · abstract, characters 451–612

Title

Post-Transcriptional Suppression of Cytosolic Ascorbate Peroxidase Expression during Pathogen-Induced Programmed Cell Death in Tobacco

Ron Mittler; Xuqiao Feng; Mira Cohen The Plant Cell 1998. doi:10.1105/tpc.10.3.461

Other claims from this paper (7)

Observation cAPX transcripts increased during PCD.
Observation cAPX protein levels declined during PCD.
Observation In vivo labeling and immunoprecipitation indicated inhibited cAPX protein synthesis.
Observation cAPX transcripts remained associated with polysomes during PCD.
Observation No cAPX protein was detected after in vitro polysome run off assays.
Mechanism The authors suggest cAPX suppression may occur at translation elongation.
Mechanism The authors infer cAPX suppression reduces H2O2 scavenging and enables H2O2 accumulation and faster PCD.

Hydrogen Peroxide-induced Cell Death in Arabidopsis: Transcriptional and Mutant Analysis Reveals a Role of an Oxoglutarate-dependent Dioxygenase Gene in the Cell Death Process 1

Show all 1 →

Observationobservedoriginal resultmeasured

Claim · model-written summary

Microarray analysis of AT-induced cell death revealed a set of new H2O2-responsive genes highly regulated in a common fashion across types of programmed cell death.

Taxon: Arabidopsis thalianaArabidopsis thalianae0
Outcome: a set of new H(2)O(2)-responsive genese1

Verbatim

e0
“Arabidopsis thaliana”
✓ located verbatim in the source · abstract, characters 284–304

e1
“Microarray analysis with a DNA chip representing 21500 genes and subsequent comparison with other PCD-related expression studies revealed a set of new H(2)O(2)-responsive genes that were highly regulated in a common fashion during different types of PCD”
✓ located verbatim in the source · abstract, characters 481–734

Title

Hydrogen Peroxide-induced Cell Death in Arabidopsis: Transcriptional and Mutant Analysis Reveals a Role of an Oxoglutarate-dependent Dioxygenase Gene in the Cell Death Process

Tsanko Gechev; Ivan Minkov; Jacques Hille IUBMB Life 2005. doi:10.1080/15216540500090793

Other claims from this paper (4)

Production of Reactive Oxygen Species, Alteration of Cytosolic Ascorbate Peroxidase, and Impairment of Mitochondrial Metabolism Are Early Events in Heat Shock-Induced Programmed Cell Death in Tobacco Bright-Yellow 2 Cells 1

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Observationobservedoriginal resultmeasured

Claim · model-written summary

Cells undergoing PCD showed an immediate burst of hydrogen peroxide and superoxide anion production in the early phase

Taxon: tobacco (Nicotiana tabacum)Nicotiana tabacume0
Outcome: burst in hydrogen peroxide (H2O2) and superoxide (O2*-) anion productione1

Verbatim

e0
“tobacco (Nicotiana tabacum) Bright-Yellow 2 cells”
✓ located verbatim in the source · abstract, characters 108–157

e1
“In the early phase, cells undergoing PCD showed an immediate burst in hydrogen peroxide (H2O2) and superoxide (O2*-) anion production”
✓ located verbatim in the source · abstract, characters 373–506

Title

Production of Reactive Oxygen Species, Alteration of Cytosolic Ascorbate Peroxidase, and Impairment of Mitochondrial Metabolism Are Early Events in Heat Shock-Induced Programmed Cell Death in Tobacco Bright-Yellow 2 Cells

Rosa Anna Vacca; Maria Concetta de Pinto; Daniela Valenti; et al. PLANT PHYSIOLOGY 2004. doi:10.1104/pp.103.035956

Other claims from this paper (13)

Intervention effect Heat treatment at 55 degrees C triggered programmed cell death in tobacco BY-2 cells, complete after 72 h
Intervention effect Cell death was prevented by the antioxidant ascorbate (ASC)
Intervention effect Cell death was prevented by superoxide dismutase (SOD)
Intervention effect Actinomycin D prevented cell death with a lower efficiency
Intervention effect Cycloheximide prevented cell death with a lower efficiency
Observation Induction of PCD resulted in gradual oxidation of endogenous ascorbate
Association PCD was accompanied by a decrease in the amount and specific activity of cytosolic ascorbate peroxidase
Observation A reduction in cAPX gene expression was found in the late PCD phase
Observation Changes in cAPX kinetic properties were found in PCD cells
Association ROS production in PCD cells was accompanied by early inhibition of glucose oxidation
Observation PCD cells showed a strong impairment of mitochondrial function, shown by an increase in cellular NAD(P)H fluorescence
Observation Mitochondria isolated from PCD cells failed to generate membrane potential and to oxidize succinate
Mechanism ROS production in early PCD may occur because of damage to the cell antioxidant system, with impairment of mitochondrial oxidative phosphorylation

S-Nitrosylation of Ascorbate Peroxidase Is Part of Programmed Cell Death Signaling in Tobacco Bright Yellow-2 Cells 1

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Intervention effectobservedoriginal resultnegativemeasured

Claim · model-written summary

Both heat shock and peroxide induced increased S-nitrosylating agents during programmed cell death.

Taxon: tobaccoNicotiana tabacume0
Treatment: heat shock (HS) or hydrogen peroxide (H2O2)e0
Outcome: S-nitrosylating agentse0
Direction: increasee0

Not reportedComparator

Verbatim

e0
“during programmed cell death (PCD), induced by both heat shock (HS) or hydrogen peroxide (H2O2) in tobacco (Nicotiana tabacum) Bright Yellow-2 cells, an increase in S-nitrosylating agents occurred”
✓ located verbatim in the source · abstract, characters 314–510

Title

S-Nitrosylation of Ascorbate Peroxidase Is Part of Programmed Cell Death Signaling in Tobacco Bright Yellow-2 Cells

M. C. de Pinto; V. Locato; A. Sgobba; et al. PLANT PHYSIOLOGY 2013. doi:10.1104/pp.113.222703

Other claims from this paper (7)

Intervention effect NO increased during both induced cell deaths, less under peroxide than heat shock.
Intervention effect GSNO increased in peroxide-treated cells.
Intervention effect GSNO decreased after heat shock.
Observation GSNO reductase activity and expression were low after peroxide and high after heat shock.
Intervention effect Both stimuli induced S-nitrosylated proteins.
Observation cAPX was S-nitrosylated at the onset of both cell deaths.
Mechanism S-nitrosylation of cAPX caused a rapid decrease in its activity.

H 2 O 2 - or NO-induced programmed death of soybean suspension cell cultures 1

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Mechanismauthor interpretationoriginal resultmeasured

Claim · model-written summary

Authors implicate a potassium ATP channel in peroxide- or NO-induced programmed cell death.

Taxon: plantsViridiplantaee0
Gene: K 1 ATP channele0
Outcome: PCDe0

Verbatim

e0
“These results point to the involvement of a K 1 ATP channel during the manifestation of PCD induced by H2O2 or NO in plants.”
✓ located verbatim in the source · abstract, characters 1654–1778

Title

H 2 O 2 - or NO-induced programmed death of soybean suspension cell cultures

Valentino Casolo; Elisa Petrussa; Angelo Vianello 2005

Other claims from this paper (14)

Intervention effect 5 mM hydrogen peroxide induced programmed cell death.
Intervention effect 20 mM hydrogen peroxide caused necrosis.
Observation ATP and glucose-6-phosphate levels remained constant during programmed cell death.
Observation ATP and glucose-6-phosphate levels significantly decreased in necrotic cells.
Intervention effect Mitochondrial oxygen consumption was slightly uncoupled after 5 mM hydrogen peroxide.
Intervention effect Mitochondrial electrical potential weakly decreased after 5 mM hydrogen peroxide.
Intervention effect KCl caused greater partial potential dissipation in treated mitochondria than controls.
Mechanism Cyclosporin A induced potential formation via matrix potassium efflux, reduced after treatment.
Observation NO-treated cells showed the same mitochondrial response pattern.
Intervention effect 20 mM hydrogen peroxide completely uncoupled mitochondrial oxygen consumption.
Intervention effect 20 mM hydrogen peroxide significantly inhibited mitochondrial potential generation.
Intervention effect 20 mM hydrogen peroxide prevented cyclosporin-dependent potential formation.
Observation Mitochondrial swelling was partly prevented in apoptotic cells and completely prevented in necrotic cells.
Association Moderate swelling accompanied outer-membrane rupture and cytochrome c release.

“H2O2-induced PCD”

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Inactivation of Carbonyl-Detoxifying Enzymes by H2O2 Is a Trigger to Increase Carbonyl Load for Initiating Programmed Cell Death in Plants 8

Spermidine Exodus and Oxidation in the Apoplast Induced by Abiotic Stress Is Responsible for H2O2 Signatures That Direct Tolerance Responses in Tobacco 7

Cobalt Alleviates GA-Induced Programmed Cell Death in Wheat Aleurone Layers via the Regulation of H2O2 Production and Heme Oxygenase-1 Expression 6

The soluble proteome of tobacco Bright Yellow-2 cells undergoing H2O2-induced programmed cell death 6

Involvement of the mitochondrial KATP+ channel in H2O2- or NO-induced programmed death of soybean suspension cell cultures 4

Post-Transcriptional Suppression of Cytosolic Ascorbate Peroxidase Expression during Pathogen-Induced Programmed Cell Death in Tobacco 2

Hydrogen Peroxide-induced Cell Death in Arabidopsis: Transcriptional and Mutant Analysis Reveals a Role of an Oxoglutarate-dependent Dioxygenase Gene in the Cell Death Process 1

Production of Reactive Oxygen Species, Alteration of Cytosolic Ascorbate Peroxidase, and Impairment of Mitochondrial Metabolism Are Early Events in Heat Shock-Induced Programmed Cell Death in Tobacco Bright-Yellow 2 Cells 1

S-Nitrosylation of Ascorbate Peroxidase Is Part of Programmed Cell Death Signaling in Tobacco Bright Yellow-2 Cells 1

H 2 O 2 - or NO-induced programmed death of soybean suspension cell cultures 1