Claim · model-written summary
The spl38 mutant is essential for hypersensitive response-like lesions and innate immunity.
- Taxon
- rice
Oryza sativae1 - Gene
- spl38e1
- Outcome
- formation of hypersensitive response-like lesions and innate immunitye1
Not reportedMaterialCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleTreatmentComparatorSettingDirectionValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e1“Here, we identified a rice (Oryza sativa) LMM, spotted leaf 38 (spl38), and demonstrated that spl38 is essential for the formation of hypersensitive response-like lesions and innate immunity”
Title
MEDIATOR SUBUNIT 16 negatively regulates rice immunity by modulating PATHOGENESIS RELATED 3 activity
Peng Zhang; Xiaoding Ma; Lina Liu; et al. PLANT PHYSIOLOGY 2023. doi:10.1093/plphys/kiad120
Other claims from this paper (14)
- Observation SPL38 encodes MEDIATOR SUBUNIT 16 (OsMED16).
- Association The spl38 mutant showed enhanced resistance to Magnaporthe oryzae.
- Association The spl38 mutant showed enhanced resistance to Xanthomonas oryzae pv. oryzae (Xoo).
- Intervention effect OsMED16-overexpressing plants showed increased susceptibility to Magnaporthe oryzae.
- Observation OsMED16-edited rice lines were phenotypically similar to the spl38 mutant.
- Intervention effect OsMED16-edited rice lines showed growth retardation and were extremely weak.
- Observation OsMED16-edited rice lines eventually died.
- Intervention effect The ospr3 osmed16 double mutants did not exhibit the lesion mimic phenotype of the spl38 mutant.
- Observation The C-terminus of OsMED16 interacts with OsPR3.
- Mechanism OsMED16 competitively represses the chitinase and chitin-binding activities of OsPR3.
- Association OsMED16 has an opposite function in plant defense relative to Arabidopsis AtMED16.
- Mechanism The opposite defense function of OsMED16 is most likely due to two amino acid substitutions between monocot and dicot MED16s.
- Mechanism OsMED16 negatively regulates cell death and immunity in rice, probably via the OsPR3-mediated chitin signaling pathway.
- Observation The spl38 mutant exhibited delayed flowering.