Claim · model-written summary
Inhibiting protein synthesis impaired ICR1 destabilization.
- Treatment
- inhibition of auxin transport and signaling, proteasome function, and protein synthesise0
- Gene
- ICR1e0
- Outcome
- Destabilization of ICR1e0
- Direction
- impairede0
Not reportedTaxonMaterialCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleComparatorSettingValueQualifier
Verbatim
e0“Destabilization of ICR1 was impaired after inhibition of auxin transport and signaling, proteasome function, and protein synthesis”
Title
Bimodal regulation of ICR1 levels generates self-organizing auxin distribution
Ora Hazak; Uri Obolski; Tomáš Prat; et al. Proceedings of the National Academy of Sciences 2014. doi:10.1073/pnas.1413918111
Other claims from this paper (10)
- Mechanism Auxin-dependent bimodal ICR1 regulation is essential for auxin maxima and gradients.
- Association ICR1 levels increase with auxin response in lateral root primordia, cotyledon tips, and provascular tissues.
- Mechanism Above critical auxin levels, ICR1 is rapidly destabilized through SCF(TIR1/AFB)-dependent signaling in the embryo hypophysis and root meristem.
- Intervention effect Ectopic ICR1 expression in the embryo hypophysis reduced auxin accumulation.
- Intervention effect Ectopic ICR1 expression in the embryo hypophysis arrested root growth.
- Observation ICR1 disappeared during root regeneration and lateral root initiation with formation of a local auxin maximum after external auxin treatments.
- Observation ICR1 disappeared transiently after gravitropic stimulation.
- Intervention effect Inhibiting auxin transport and signaling impaired ICR1 destabilization.
- Intervention effect Inhibiting proteasome function impaired ICR1 destabilization.
- Method / resource The model simulated in vivo-like auxin distribution, rootward flux, and shootward reflux without preexisting tissue polarity.