Claim · model-written summary
Identified infection-specific proteins included mitochondrial-processing peptidase subunit alpha isoform B, T-complex protein 1 subunit eta and glutathione S-transferase-like protein.
- Taxon
- Japanese birche1
- Organ / stage
- calluse1
- Interactor
- Inonotus obliquus strain IO‐U1 (NBRC 113406)
Inonotus obliquuse1pathogen - Outcome
- mitochondrial‐processing peptidase subunit alpha isoform B (spot ID 1578), T‐complex protein 1 subunit eta (spot ID 356), glutathione S ‐transferase‐like protein (spot ID 1121)e0
Not reportedMaterialGeneCompoundSecond interactorSecond interactor roleTreatmentComparatorSettingDirectionValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“mitochondrial‐processing peptidase subunit alpha isoform B (spot ID 1578), T‐complex protein 1 subunit eta (spot ID 356), glutathione S ‐transferase‐like protein (spot ID 1121)”
e1“Japanese birch ( Betula platyphylla var. japonica plantlet No. 8) callus infected with a canker‐rot fungus Inonotus obliquus strain IO‐U1 (NBRC 113406)”
Title
Retno Agnestisia; Rei Chino; Ikumi Nezu; et al. Forest Pathology 2025. doi:10.1111/efp.70051
Other claims from this paper (6)
- Observation Proteome analysis detected 134 infection-specific protein spots in Japanese birch callus.
- Observation Highly expressed infection-specific proteins included protochlorophyllide reductase chloroplastic, enolase and mitochondrial-processing peptidase subunit alpha-like.
- Observation Identified infection-specific proteins included partial glutathione S-transferase-like protein, WALLS ARE THIN 1-like and 1 Sc-3.
- Mechanism Early infected Japanese birch callus is interpreted as inducing defense proteins related to photosynthesis, energy production and mitochondrial protein import.
- Mechanism Early infected birch callus is interpreted as inducing defense proteins related to protein folding, detoxification and secondary cell wall formation.
- Mechanism Early infected birch callus is interpreted as inducing PR-10 protein as a defense response.