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“H2O2-induced PCD”

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1990 2000 ’10 ’20

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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.

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 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.

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.

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.

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

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)

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.

Intervention effectobservedoriginal resultmeasured

Claim · model-written summary

S-pao tobacco plants had higher H2O2 levels under salt stress.

Taxon: tobaccoNicotiana tabacume0
Material: S-pao plantse3
Treatment: salt stresse2
Outcome: H2O2 levelse3
Direction: highere3

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

e2
“Upon salt stress, plants secreted spermidine (Spd) into the apoplast, where it was oxidized by the apoplastic PAO, generating H2O2”
✓ located verbatim in the source · abstract, characters 493–623

e3
“S-pao plants, with higher H2O2 levels, failed to accumulate stress-responsive mRNAs, inducing PCD instead”
✓ located verbatim in the source · abstract, characters 1033–1138

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

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“H2O2-induced PCD”

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