Claim · model-written summary
The rcd1 mutant is sensitive to ozone and apoplastic superoxide.
- Taxon
- Arabidopsis thaliana
Arabidopsis thalianat0 - Material
- rcd1e0
- Treatment
- O3 and apoplastic superoxidee0
- Outcome
- sensitivee0
Not reportedGeneCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleComparatorSettingDirectionValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
t0“Arabidopsis thaliana”
e0“rcd1 is sensitive against O3 and apoplastic superoxide”
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 Functional SA signaling was needed for full protein levels and activation of AtMPK3.
- 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 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.