Innate immunity
Plant TIR domain binds viral elicitor
Open access · cc by · source: Europe PMC
Tobacco N protein’s TIR domain is critical for association with TMV p50 elicitor.
Study at a glance
- Design
- Animal / in-vitro — Co-expression domain mapping of N and TMV p50 in N. benthamiana
- N
- Plant molecular genetics / protein-association assays — no single sample N
- Population
- Nicotiana benthamiana expressing tagged N and TMV p50
- Outcome
- TIR-domain requirement for N–p50 association and HR cell death
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
Co-expression triggers HR in 2 days; N and p50 are cytoplasmic; the TIR domain of N is critical for association with p50.
Methodology
Tagged N and TMV p50, co-expressed them in N. benthamiana, and mapped domains needed for physical association and HR cell death.
Limitations
Does not solve a full atomic structure of the N–p50 complex.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
TIR-domain architecture participates in innate association/signaling logic.
TIR-domain association findings add receptor-proximal innate signaling context to nucleic-acid sensor → IFN pathways.
Evidence for the claim as stated.
Tagged tobacco N and TMV p50 co-expressed in N. benthamiana associated in the cytoplasm; the TIR domain of N was critical for that association, and co-expression triggered hypersensitive-response cell death in two days. Domain mapping of a physical association is a classic immunoblot/co-IP use, not an atomic structure of the complex.
Evidence for the claim as stated.
Westerns here answer different biochemical questions. Caveolar work asks which subunits co-purify; N–p50 asks which domain is required for association and HR; USP8 asks whether Smo is ubiquitinated; spike work asks whether glycan occupancy and palmitoylation change S2 mobility and trafficking. A darker band is not a universal 'more protein' story across those designs.
Evidence for the claim as stated.
Several confocal-tagged papers use imaging only as a supporting localisation. APEX2 defined 22 OMM and 72 ERM cytosol-facing proteins by mass spectrometry; caveolar-coat work is biochemical stoichiometry plus ultrastructure (caveolin–cavin complex excluding EHD2/pacsin 2); N and TMV p50 were cytoplasmic in N. benthamiana with TIR-dependent association and HR in two days. Those localisation notes are not confocal trafficking movies.
Evidence for the claim as stated.
APEX2, caveolar ultrastructure, and plant TIR–p50 association are weaker confocal examples: proximity biotinylation, electron-microscopy-scale coat structure, and cytoplasmic HR biochemistry. Citing them as confocal method papers overstates the imaging.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Westerns here answer different biochemical questions. Caveolar work asks which subunits co-purify; N–p50 asks which domain is required for association and HR; USP8 asks whether Smo is ubiquitinated; spike work asks whether glycan occupancy and palmitoylation change S2 mobility and trafficking. A darker band is not a universal 'more protein' story across those designs.
- Supports · What proteins build the caveolar coat?
- Supports · How does USP8 turn on Smoothened?
- Supports · Spike glycosylation and palmitoylation trafficking
APEX2, caveolar ultrastructure, and plant TIR–p50 association are weaker confocal examples: proximity biotinylation, electron-microscopy-scale coat structure, and cytoplasmic HR biochemistry. Citing them as confocal method papers overstates the imaging.
- Supports · Mapping the faces of mitochondria and ER
- Supports · What proteins build the caveolar coat?
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Same topic cluster — not a recommendation engine.