Search claims · PlantClaims

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)

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.

Mechanismhypothesisoriginal resultpositivebasis n/a

Claim · model-written summary

H2O2 may mediate salicylic acid in preventing heat-induced pollen abortion by inhibiting tapetum PCD.

Taxon: riceOryza sativat0
Compound: H 2 O 2e2
Outcome: pollen abortione2

Verbatim

t0
“rice”
✓ located verbatim in the source · title, characters 43–47

e2
“We suggest that H 2 O 2 may play an important role in mediating SA to prevent pollen abortion caused by heat stress through inhibiting the tapetum PCD”
✓ located verbatim in the source · abstract, characters 1464–1614

Title

Salicylic acid reverses pollen abortion of rice caused by heat stress

Baohua Feng; Caixia Zhang; Tingting Chen; et al. BMC Plant Biology 2018. doi:10.1186/s12870-018-1472-5

Other claims from this paper (6)

Intervention effect Under heat stress, salicylic acid decreased reactive oxygen species accumulation in anthers.
Intervention effect Salicylic acid prevented tapetum programmed cell death and degradation.
Mechanism The genes EAT1, MIL2 and DTM1 are involved in tapetum development in this process.
Intervention effect Exogenous salicylic acid spray gave significantly higher pollen viability under heat stress than control sprays.
Intervention effect Salicylic acid or PAC plus H2O2 treatment sharply increased H2O2 relative to other treatments.
Intervention effect Under control conditions, salicylic acid treatments showed no significant difference in pollen viability or seed-setting rate.

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.

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.

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 resultpositivemeasured

Claim · model-written summary

JL54 induced rapid H2O2 accumulation, lignin deposition and localized programmed cell death in Larix.

Taxon: Larix olgensisLarix gmelinii var. olgensise1
Treatment: JL54e0
Outcome: hydrogen peroxide (H2O2) accumulation, extensive lignin deposition, and localized programmed cell death (PCD)e0
Direction: accumulatione0

Not reportedComparator

Verbatim

e0
“JL54-induced rapid hydrogen peroxide (H2O2) accumulation, extensive lignin deposition, and localized programmed cell death (PCD)”
✓ located verbatim in the source · abstract, characters 611–739

e1
“Larix olgensis”
✓ located verbatim in the source · abstract, characters 0–14

Title

Integrative Transcriptomic and Biochemical Profiling Reveals Bacillus amyloliquefaciens JL54 Primes Larix olgensis Defenses Against Neofusicoccum laricinum Attack

Xiangyu Zhao; Fengze Yang; Lingyu Kong; et al. Plants 2026. doi:10.3390/plants15081181

Other claims from this paper (8)

Intervention effect JL54 pretreatment reduced shoot blight disease incidence in Larix by 12.5%.
Intervention effect JL54 pretreatment achieved 43.75% shoot blight control efficacy in Larix.
Intervention effect JL54 pretreatment maintained Larix host vigor.
Observation At 0 h post-inoculation, Larix defense showed upregulation of cutin, suberin and wax biosynthesis pathways.
Observation At 12 h post-inoculation, Larix responses were dominated by ribosome and proteostasis related pathways.
Intervention effect JL54 colonization reduced Larix malondialdehyde content by 27.2%.
Intervention effect JL54 colonization significantly increased POD, PAL and GST defense enzyme activities in Larix.
Mechanism Phytohormone profiling implicated JA signaling as central to JL54-induced systemic resistance and preceding pathogen containment.

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

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.

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.

“H2O2-induced PCD”

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