Claim · model-written summary
Host oxygen consumption peaked 48 hours after infection.
- Taxon
- Thalassia testudinum
Thalassia testudinumt0 - Interactor
- Labyrinthula sp.Labyrinthulat0pathogen
- Outcome
- host oxygen consumptione0
- Direction
- higheste0
- Qualifier
- 48-hr post-infectione0
Not reportedMaterialGeneCompoundOrgan / stageSecond interactorSecond interactor roleTreatmentComparatorSettingValue
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
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Verbatim
e0“By 48-hr post-infection, host oxygen consumption, internal reactive oxygen concentrations, and caspase-3 proteolytic activity reached their highest levels”
t0“Thalassia testudinum) undergoes a coordinated hypersensitive response when challenged with pathogenic Labyrinthula sp.”
Title
Ava Larson; Daniel L. Martin; Cliff Ross Plant Physiology and Biochemistry 2025. doi:10.1016/j.plaphy.2025.110427
Other claims from this paper (13)
- Intervention effect Labyrinthula infection induced lesion progression in turtlegrass.
- Intervention effect Infection altered host oxidative metabolism and induced defense metabolites.
- Observation Internal reactive oxygen concentrations peaked 48 hours after infection.
- Observation Caspase-3 activity peaked 48 hours after infection.
- Observation Reactive oxygen species were detected in turtlegrass lesions.
- Observation Nitric oxide was detected in turtlegrass lesions.
- Intervention effect Diphenyleneiodonium regulated hydrogen peroxide production and lesion expansion.
- Intervention effect Catalase regulated hydrogen peroxide production and lesion expansion.
- Intervention effect c-PTIO regulated hydrogen peroxide production and lesion expansion.
- Intervention effect Succinic acid concentration increased after infection.
- Intervention effect 3-phenylpropionic acid concentration increased after infection.
- Intervention effect Methyl p-coumarate concentration increased after infection.
- Mechanism The authors attribute lesions to host hypersensitive cell death and direct pathogen tissue degradation.