Search claims · PlantClaims

Mechanismauthor interpretationoriginal resultmeasured

Claim · model-written summary

Authors suggest COI1-dependent JA signaling enhances toxin-induced PCD through leaf redox status, hormone pathways or PCD components.

Taxon: tomatoSolanum lycopersicumt0
Gene: COI1e0
Outcome: AAL toxin induced PCDe0
Qualifier: regulating the redox status of the leaves, other phytohormone pathways and/or important PCD componentse0

Verbatim

e0
“COI1-dependent JA pathway enhances AAL toxin induced PCD through regulating the redox status of the leaves, other phytohormone pathways and/or important PCD components”
✓ located verbatim in the source · abstract, characters 1175–1342

t0
“Tomato”
✓ located verbatim in the source · title, characters 78–84

Title

Critical Role of COI1-Dependent Jasmonate Pathway in AAL toxin induced PCD in Tomato Revealed by Comparative Proteomics

Min Zhang; Jin Koh; Lihong Liu; et al. Scientific Reports 2016. doi:10.1038/srep28451

Other claims from this paper (6)

Intervention effect AAL toxin induces PCD in susceptible tomato leaves.
Mechanism Jasmonate promoted AAL toxin-induced PCD via COI1-dependent enhancement of ROS.
Method / resource Proteomics identified 10367 proteins in tomato leaves.
Observation AAL toxin and JA elicited differential expression of 2670 proteins.
Observation Comparison of jai1 and wild type identified COI1-dependent proteins in redox, ceramide and hormone pathways.
Observation Autophagy, PCD and DNA damage related proteins were identified.

Mechanismobservedoriginal resultmeasured

Claim · model-written summary

UV-induced PCD required light.

Taxon: ArabidopsisArabidopsist0
Outcome: PCDe0
Qualifier: requires lighte0

Verbatim

e0
“UV induction of PCD requires light”
✓ located verbatim in the source · abstract, characters 394–428

t0
“Arabidopsis”
✓ located verbatim in the source · title, characters 64–75

Title

Caspase-like activities and UV-induced programmed cell death in Arabidopsis

V Rotari; A Gordon; R He; et al. BMC Plant Biology 2005. doi:10.1186/1471-2229-5-s1-s18

Other claims from this paper (5)

Intervention effect UV induced apoptotic-like cellular changes.
Observation DEVDase activity was induced within 30 minutes and peaked at one hour.
Intervention effect DEVDase was insensitive to broad-range cysteine protease inhibitors.
Intervention effect Caspase inhibitors suppressed DNA fragmentation and cell death.
Mechanism YVADase and DEVDase may mediate DNA fragmentation under UV overexposure.

Mechanismhypothesisoriginal resultmeasured

Claim · model-written summary

The authors suggest suppressed PCD-related gene expression may mediate delayed PCD under EPH1 suppression.

Taxon: Japanese morning gloryIpomoea nilt0
Organ / stage: petalse0
Gene: PCD-related genese0
Outcome: suppression of the expression of PCD-related genese0

Verbatim

e0
“possibly through suppression of the expression of PCD-related genes, including genes for plant caspase and autophagy in the petals”
✓ located verbatim in the source · abstract, characters 783–913

t0
“Japanese morning glory”
✓ located verbatim in the source · title, characters 92–114

Title

Identification of a NAC transcription factor, EPHEMERAL1, that controls petal senescence in Japanese morning glory

Kenichi Shibuya; Keiichi Shimizu; Tomoko Niki; et al. The Plant Journal 2014. doi:10.1111/tpj.12605

Other claims from this paper (5)

Mechanism EPH1 positively regulates programmed cell death during Japanese morning glory petal senescence.
Observation EPH1 expression is induced independently of ethylene signaling.
Intervention effect Suppressing EPH1 kept Japanese morning glory flowers in bloom until the second day.
Intervention effect Suppressing EPH1 expression delayed progression of petal programmed cell death.
Mechanism EPH1 may regulate ethylene-accelerated petal senescence.

Mechanismobservedoriginal resultmeasured

Claim · model-written summary

Pericarp PCD depends on ATG8-mediated autophagy.

Taxon: WheatTriticum aestivumt0
Gene: ATG8e0
Outcome: PCDe0
Qualifier: autophagye0

Verbatim

e0
“PCD was also found to rely on ATG8 -mediated autophagy”
✓ located verbatim in the source · abstract, characters 1279–1333

t0
“Wheat Grains”
✓ located verbatim in the source · title, characters 44–56

Title

Programmed Degradation of Pericarp Cells in Wheat Grains Depends on Autophagy

Yong-Bo Li; Mei Yan; De-Zhou Cui; et al. Frontiers in Genetics 2021. doi:10.3389/fgene.2021.784545

Other claims from this paper (9)

Observation Pericarp was thinnest at the spike top, intermediate in the middle and thickest at the bottom.
Mechanism Pericarp cell-layer number corresponded to thickness differences and decreased through programmed cell death.
Observation ATG8-PE expression increased before autophagy structures appeared.
Observation Autophagy structures appeared following increased ATG8-PE expression.
Intervention effect Interference with ATG8 inhibited pericarp programmed cell death.
Intervention effect Interference with ATG8 increased pericarp thickness.
Intervention effect ATG8 interference resulted in small premature grains.
Observation Autophagy and programmed cell death coexist during early wheat pericarp development.
Observation Autophagy and PCD increased from spike bottom to top.

Mechanismauthor interpretationoriginal resultbasis n/a

Claim · model-written summary

KOD is a novel pro-PCD component of the Arabidopsis cell death machinery and the first plant peptide involved in a form of developmental PCD.

Taxon: ArabidopsisArabidopsise0
Gene: KODe0
Outcome: novel pro-PCD component of the Arabidopsis cell death machinerye0
Qualifier: the first plant peptide to be involved with a form of developmental PCDe0

Verbatim

e0
“KOD appears to be a novel pro-PCD component of the Arabidopsis cell death machinery and represents the first plant peptide to be involved with a form of developmental PCD”
✓ located verbatim in the source · abstract, characters 1600–1770

Title

Is the Arabidopsis peptide KISS OF DEATH an inducer of Programmed Cell Death

Bennett Young Research Explorer (The University of Manchester) 2010

Other claims from this paper (11)

Mechanismauthor interpretationoriginal resultnegativemeasured

Claim · model-written summary

The bp1 signaling change advanced anther-wall PCD.

Taxon: riceOryza sativat0
Organ / stage: anther wallse0
Outcome: programmed cell death (PCD) of anther wallse0
Qualifier: thereby advancinge0

Verbatim

e0
“thereby advancing programmed cell death (PCD) of anther walls”
✓ located verbatim in the source · abstract, characters 808–869

t0
“rice”
✓ located verbatim in the source · title, characters 114–118

Title

BOTRYOID POLLEN 1 regulates ROS-triggered PCD and pollen wall development by controlling UDP-sugar homeostasis in rice

Huiqiong Chen; Shuqing Zhang; Ruiqi Li; et al. The Plant Cell 2023. doi:10.1093/plcell/koad181

Other claims from this paper (9)

Mechanism BP1 encodes a UGE that regulates UDP-sugar homeostasis and rice anther development.
Intervention effect Loss of BP1 caused massive UDP-Glc accumulation.
Intervention effect Loss of BP1 disrupted other UDP-sugars.
Mechanism Elevated UDP-Glc and its derivatives in bp1 may induce NADPH oxidase gene expression.
Mechanism Higher UDP-Glc in bp1 may cause premature ROS accumulation.
Mechanism The bp1 signaling change delayed the end of tapetal degradation.
Mechanism UDP-Glc accumulation caused abnormal callose degradation and adhesive microspores.
Mechanism The UDP-sugar metabolism pathway participates in intine formation.
Mechanism The UDP-sugar metabolism pathway participates in the initial extine framework.

Mechanismauthor interpretationoriginal resultmeasured

Claim · model-written summary

SIC regulates SA-triggered PCD.

Taxon: ArabidopsisArabidopsise1
Gene: SICe0
Compound: SAe0
Outcome: SA-triggered PCDe0

Not reportedDirection

Verbatim

e0
“SIC is involved in regulating SA-triggered PCD”
✓ located verbatim in the source · abstract, characters 1136–1182

t0
“SICKLE”
✓ located verbatim in the source · title, characters 11–17

e1
“In Arabidopsis (Arabidopsis thaliana)”
✓ located verbatim in the source · abstract, characters 175–212

Title

Absence of SICKLE triggers programed cell death by disturbing alternative splicing and decay of mRNAs

Chengyun Wu; Weibo Zhen; Xingsong Wang; et al. PLANT PHYSIOLOGY 2023. doi:10.1093/plphys/kiad192

Other claims from this paper (9)

Mechanism SIC represses programmed cell death.
Observation The sic-4 mutant accumulated lariat intronic RNAs.
Observation The sic-4 mutant exhibited PCD.
Intervention effect DBR1 overexpression reduced lariRNAs in sic-4.
Intervention effect DBR1 overexpression suppressed PCD in sic-4.
Observation The dbr1-2 mutant exhibited PCD.
Observation The sic-4 mutation disturbed splicing and decay of mRNAs associated with SA homeostasis.
Observation SA increased dramatically in sic-4.
Intervention effect Disrupting SA biosynthesis and signaling suppressed PCD in sic-4.

Mechanismobservedoriginal resultmeasured

Claim · model-written summary

SA-independent and SA-dependent processes were involved in ozone-induced PCD in rcd1.

Taxon: Arabidopsis thalianaArabidopsis thalianat0
Material: rcd1e0
Compound: SAe0
Outcome: O3-induced PCDe0

Verbatim

t0
“Arabidopsis thaliana”
✓ located verbatim in the source · title, characters 27–47

e0
“SA independent and dependent processes were involved in the O3-induced PCD in rcd1”
✓ located verbatim in the source · abstract, characters 3256–3338

Title

Ozone-induced signaling in Arabidopsis thaliana

Reetta Ahlfors Työväentutkimus Vuosikirja 2008

Other claims from this paper (19)

Mechanismauthor interpretationoriginal resultmeasured

Claim · model-written summary

The results suggest GA regulates exine formation and tapetal PCD.

Taxon: riceOryza sativat0
Outcome: exine formation and the PCD of tapetal cellse0
Qualifier: GAe0

Verbatim

e0
“GA regulates exine formation and the PCD of tapetal cells”
✓ located verbatim in the source · abstract, characters 1334–1391

t0
“Rice”
✓ located verbatim in the source · title, characters 44–48

Title

Gibberellin Modulates Anther Development in Rice via the Transcriptional Regulation of GAMYB

Koichiro Aya; Miyako Ueguchi-Tanaka; Maki Kondo; et al. The Plant Cell 2009. doi:10.1105/tpc.108.062935

Other claims from this paper (7)

Observation GA-deficient, GA-insensitive, and gamyb mutants had common tapetal PCD defects.
Observation The same mutants had defects in exine and Ubisch body formation.
Association GAMYB was involved in nearly all GA-regulated gene expression in rice anthers.
Observation GAMYB interacted with promoter binding motifs in vitro.
Intervention effect Mutation of promoter motifs reduced GUS expression in anthers.
Intervention effect CYP703A3 knockout had gamyb-like defects in exine and Ubisch body formation.
Mechanism The results suggest direct CYP703A3 activation by GAMYB is key to exine formation.

Mechanismhypothesisoriginal resultbasis n/a

Claim · model-written summary

Mitochondria may be a possible trigger for caspase-like proteases during PCD in the lace plant.

Taxon: lace plante6
Gene: CLPse6
Outcome: PCDe6
Qualifier: mitochondria as a possible triggere6

Verbatim

e6
“suggesting the mitochondria as a possible trigger for CLPs during PCD in the lace plant”
✓ located verbatim in the source · abstract, characters 1476–1563

Title

Unveiling Interactions among Mitochondria, Caspase-Like Proteases, and the Actin Cytoskeleton during Plant Programmed Cell Death (PCD)

Christina E. N. Lord; Adrian N. Dauphinee; Rebecca L. Watts; et al. PLoS ONE 2013. doi:10.1371/journal.pone.0057110

Other claims from this paper (7)

Observation YVADase (caspase-1) activity was higher in the very early stages of perforation formation.
Intervention effect Actin depolymerization with Lat B caused no change in YVADase activity.
Intervention effect In vivo inhibition of YVADase activity prevented PCD and actin breakdown.
Intervention effect The mitochondrial pore inhibitor CsA significantly decreased YVADase activity.
Intervention effect The mitochondrial pore inhibitor CsA prevented PCD and actin breakdown.
Mechanism Actin is likely a substrate for caspase-like proteases (CLPs) during PCD.
Observation Bundling and subsequent breakdown of actin followed the YVADase activity during perforation formation.

“PCD”

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