Claim · model-written summary
Labyrinthula infection induced lesion progression in turtlegrass.
- Taxon
- Thalassia testudinum Banks ex König
_(South_Pigeon_Creek_estuary%2C_San_Salvador_Island%2C_Bahamas)_3_(15859724719).jpg?width=60)
Thalassia testudinume0 - Treatment
- Infectione0
- Interactor
- Labyrinthula sp.Labyrinthulae0pathogent0
- Outcome
- lesion progressione0
- Direction
- inducee0
Not reportedMaterialGeneCompoundOrgan / stageSecond interactorSecond interactor roleComparatorSettingValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
_(South_Pigeon_Creek_estuary%2C_San_Salvador_Island%2C_Bahamas)_3_(15859724719).jpg?width=500)
Verbatim
e0“Infection of the marine subtropical seagrass Thalassia testudinum Banks ex König by pathogenic Labyrinthula sp. was found to induce lesion progression”
t0“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 Infection altered host oxidative metabolism and induced defense metabolites.
- Observation Host oxygen consumption peaked 48 hours after infection.
- 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.