Claim · model-written summary
The ssi4 sequence had one amino acid substitution in the NBS compared with wild type.
- Taxon
- Arabidopsis
Arabidopsist0 - Gene
- ssi4e0
- Outcome
- single amino acid substitution in the NBSe0
- Comparator
- corresponding wild-type sequencee0
Not reportedMaterialCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleTreatmentSettingDirectionValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“Comparison between ssi4 and the corresponding wild-type sequence revealed a single amino acid substitution in the NBS.”
t0“Arabidopsis”
Title
Yumiko Shirano; Pradeep Kachroo; Jyoti Shah; et al. The Plant Cell 2002. doi:10.1105/tpc.005348
Other claims from this paper (14)
- Intervention effect The ssi4 mutation caused constitutive PR gene expression.
- Intervention effect The ssi4 mutation induced salicylic acid accumulation.
- Intervention effect The ssi4 mutation triggered programmed cell death.
- Intervention effect The ssi4 mutation enhanced resistance to bacterial and oomycete pathogens.
- Observation Map-based cloning identified ssi4 as encoding a putative TIR-NBS-LRR resistance protein.
- Mechanism SA and EDS1 were required for ssi4-induced PR-1 expression.
- Mechanism SA and EDS1 were required for enhanced disease resistance in ssi4.
- Mechanism SA and EDS1 were required for increased SSI4 and EDS1 transcript accumulation in ssi4.
- Association High ssi4 transcript levels correlated with the mutant phenotype.
- Intervention effect Wild-type SSI4 overexpression did not induce stunting, spontaneous lesions, or increased PR-1 expression.
- Mechanism The authors propose that the NBS substitution constitutively activates the R protein.
- Intervention effect SA treatment induced SSI4, RPP1, and RPS4 expression.
- Intervention effect SA treatment had little effect on RPM1 and RPS2 expression.
- Mechanism The authors suggest that SA upregulates certain resistance genes.