Claim · model-written summary
Ectopic CYP83A1 overexpression rescued the rnt1-1 phenotype.
- Taxon
- Arabidopsis
Arabidopsise1 - Material
- rnt1-1e0
- Treatment
- ectopic overexpression of CYP83A1 using a 35S promotere0
- Gene
- CYP83A1e0
- Outcome
- rnt1-1 phenotypee0
- Direction
- rescuese0
Not reportedCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleComparatorSettingValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“ectopic overexpression of CYP83A1 using a 35S promoter rescues the rnt1-1 phenotype”
e1“CYP83B1 in Arabidopsis”
Title
Søren Bak; René Feyereisen PLANT PHYSIOLOGY 2001. doi:10.1104/pp.127.1.108
Other claims from this paper (9)
- Association CYP83A1 and CYP83B1 share 63% amino acid sequence identity.
- Intervention effect Endogenous-promoter CYP83A1 expression did not prevent the auxin excess phenotype of rnt1-1.
- Intervention effect Endogenous-promoter CYP83A1 expression did not prevent the indole glucosinolate deficit of rnt1-1.
- Mechanism CYP83A1 and CYP83B1 both convert indole-3-acetaldoxime to a thiohydroximate adduct.
- Association Indole-3-acetaldoxime had 50-fold greater affinity for CYP83B1 than CYP83A1.
- Mechanism Both CYP83 enzymes metabolized phenylalanine- and tyrosine-derived aldoximes.
- Mechanism Indole-3-acetaldoxime was identified as the physiological substrate of CYP83B1 but not CYP83A1.
- Mechanism CYP83A1 catalyzed initial aldoxime conversion for glucosinolates not derived from tryptophan.
- Observation Putative auxin-responsive promoter elements were present in CYP83B1 but absent from CYP83A1.