Claim · model-written summary
AtOSM34 overexpression promotes infection.
- Taxon
- TuMV
Turnip mosaic viruse0 - Treatment
- overexpressione0
- Interactor
- Arabidopsis
Arabidopsise1host - Gene
- AtOSM34e0
- Outcome
- viral infectione0
- Direction
- promotese0
Not reportedMaterialCompoundOrgan / stageSecond interactorSecond interactor roleComparatorSettingValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“Knockdown of AtOSM34 inhibits TuMV infection, whereas its overexpression promotes viral infection.”
e1“TuMV-Arabidopsis pathosystem”
Title
Rongrong He; Yinzi Li; Mark A. Bernards; et al. New Phytologist 2024. doi:10.1111/nph.20233
Other claims from this paper (11)
- Observation AtOSM34 is localized at plasmodesmata.
- Observation AtOLP is localized at plasmodesmata.
- Intervention effect TuMV infection upregulates AtOSM34 expression.
- Intervention effect TuMV infection downregulates AtOLP expression.
- Intervention effect AtOLP deficiency does not affect viral RNA accumulation.
- Intervention effect AtOLP overexpression does not affect viral RNA accumulation.
- Intervention effect AtOSM34 knockdown inhibits TuMV infection.
- Mechanism AtOSM34 reduces plasmodesmal callose deposition to promote viral movement.
- Mechanism AtOSM34 targets the viral replication complex to enhance replication.
- Mechanism AtOSM34 suppresses the ROS-mediated antiviral response.
- Mechanism The authors infer that TuMV selectively subverts AtOSM34 to aid infection.