Claim · model-written summary
Functional SA signaling was needed for full protein levels and activation of AtMPK3.
- Taxon
- Arabidopsis thaliana
Arabidopsis thalianat0 - Gene
- AtMPK3e0
- Compound
- SAe0
- Outcome
- full protein levels and activation of AtMPK3e0
Not reportedMaterialOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleTreatmentComparatorSettingDirectionValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
t0“Arabidopsis thaliana”
e0“Functional SA signaling was shown to be needed for the full protein levels and activation of AtMPK3”
Title
Ozone-induced signaling in Arabidopsis thaliana
Reetta Ahlfors Työväentutkimus Vuosikirja 2008
Other claims from this paper (19)
- Observation MAPKs were activated at the beginning of ozone exposure in Arabidopsis.
- Observation The activities of AtMPK3 and AtMPK6 reached their maximum at 1 and 2 hours after the start of ozone exposure, respectively.
- Observation MAPK activity decreased back to clean air levels 8 hours after the start of ozone exposure.
- Observation AtMPK3 and AtMPK6 were translocated to the nucleus at the beginning of ozone exposure.
- Mechanism AtMPK3 and AtMPK6 activation was not dependent on ethylene signaling.
- Mechanism Jasmonic acid had an impact on AtMPK3 protein levels and AtMPK3 activity.
- Observation RCD1 was shown to encode a gene with WWE and ADP-ribosylation domains.
- Observation The rcd1 mutant is sensitive to ozone and apoplastic superoxide.
- Observation The rcd1 mutant is tolerant to paraquat, which produces superoxide in the chloroplast.
- Observation The rcd1 mutant is partially insensitive to glucose and has altered hormone responses (ABA insensitivity, reduced jasmonic acid and ethylene sensitivity).
- Observation The rcd1 mutant exhibits the classical features of programmed cell death in response to ozone.
- Observation The rcd1 mutant produced extensive amounts of salicylic acid and jasmonic acid in response to ozone.
- Mechanism SA-independent and SA-dependent processes were involved in ozone-induced PCD in rcd1.
- Mechanism Increased sensitivity to jasmonic acid led to increased sensitivity to ozone in the double mutant studies.
- Observation The rcd1 mutant had alterations in MAPK signature resembling those of mutants defective in SA and JA signaling.
- Observation NO accumulated transiently at the beginning of ozone exposure, and at late time points NO accumulation coincided with HR-like lesions.
- Mechanism NO modified defense gene expression, such as SA and ethylene biosynthetic genes.
- Observation The rcd1 mutant produced more NO in control conditions.
- Mechanism NO was involved in ozone-induced signaling leading to attenuation of SA biosynthesis and other defense-related genes.