Claim · model-written summary
HCl at matched pH decreased performance less than H2C2O4.
- Taxon
- tobacco
Nicotiana tabacumt0 - Treatment
- HCle0
- Outcome
- photosynthetic performancee0
- Direction
- much less decreasee0
- Comparator
- H2C2O4e0
Not reportedMaterialGeneCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleSettingValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“treatment with H3PO4 and HCl at the same pH as H2C2O4 caused much less decrease in photosynthetic performance than H2C2O4 did.”
t0“tobacco leaves”
Title
Cheng Yang; Zishan Zhang; Huiyuan Gao; et al. BMC Plant Biology 2014. doi:10.1186/s12870-014-0240-4
Other claims from this paper (16)
- Intervention effect Sclerotinia infection reduced O2 evolution and Fv/Fm under high light.
- Intervention effect H2C2O4 at pH 4 significantly decreased photosynthetic performance.
- Intervention effect H3PO4 at matched pH decreased performance less than H2C2O4.
- Mechanism Acidity explained only part of the photosynthesis decrease.
- Intervention effect K2C2O4 reduced Fv/Fm by about 70% of the effect of H2C2O4.
- Intervention effect K2C2O4 did not further reduce photosynthetic performance when D1 synthesis was fully inhibited.
- Mechanism Oxalate represses D1 synthesis and thereby inhibits PSII.
- Intervention effect K2C2O4 inhibited RuBP regeneration.
- Intervention effect K2C2O4 inhibited carboxylation efficiency.
- Intervention effect K2C2O4 did not further decrease performance with carbon assimilation inhibited.
- Mechanism C2O4(2-) partially inhibits PSII through carbon assimilation repression.
- Intervention effect C2O4(2-) inhibited PSII activity.
- Intervention effect C2O4(2-) did not inhibit PSI activity.
- Mechanism Oxalate damage to photosynthetic apparatus exceeds the effect of acidity.
- Mechanism Oxalate inhibition of PSII, RuBP regeneration and carboxylation leads to excess ROS.
- Mechanism ROS may accelerate PSII photoinhibition through D1 synthesis inhibition.