PMID- 23418559
OWN - NLM
STAT- MEDLINE
DCOM- 20130827
LR  - 20240313
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 2
DP  - 2013
TI  - Nitric oxide deficiency accelerates chlorophyll breakdown and stability loss of 
      thylakoid membranes during dark-induced leaf senescence in Arabidopsis.
PG  - e56345
LID - 10.1371/journal.pone.0056345 [doi]
LID - e56345
AB  - Nitric oxide (NO) has been known to preserve the level of chlorophyll (Chl) 
      during leaf senescence. However, the mechanism by which NO regulates Chl 
      breakdown remains unknown. Here we report that NO negatively regulates the 
      activities of Chl catabolic enzymes during dark-induced leaf senescence. The 
      transcriptional levels of the major enzyme genes involving Chl breakdown pathway 
      except for RED CHL CATABOLITE REDUCTASE (RCCR) were dramatically up-regulated 
      during dark-induced Chl degradation in the leaves of Arabidopsis NO-deficient 
      mutant nos1/noa1 that exhibited an early-senescence phenotype. The activity of 
      pheide a oxygenase (PAO) was higher in the dark-induced senescent leaves of 
      nos1/noa1 compared with wild type. Furthermore, the knockout of PAO in nos1/noa1 
      background led to pheide a accumulation in the double mutant pao1 nos1/noa1, 
      which retained the level of Chl during dark-induced leaf senescence. The 
      accumulated pheide a in darkened leaves of pao1 nos1/noa1 was likely to inhibit 
      the senescence-activated transcriptional levels of Chl catabolic genes as a 
      feed-back inhibitory effect. We also found that NO deficiency led to decrease in 
      the stability of photosynthetic complexes in thylakoid membranes. Importantly, 
      the accumulation of pheide a caused by PAO mutations in combination with NO 
      deficiency had a synergistic effect on the stability loss of thylakoid membrane 
      complexes in the double mutant pao1 nos1/noa1 during dark-induced leaf 
      senescence. Taken together, our findings have demonstrated that NO is a novel 
      negative regulator of Chl catabolic pathway and positively functions in 
      maintaining the stability of thylakoid membranes during leaf senescence.
FAU - Liu, Fang
AU  - Liu F
AD  - The National Key Laboratory of Plant Molecular Genetics and National Center for 
      Plant Gene Research (Shanghai), Institute of Plant Physiology & Ecology, Shanghai 
      Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 
      People's Republic of China.
FAU - Guo, Fang-Qing
AU  - Guo FQ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130213
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (Arabidopsis Proteins)
RN  - 1406-65-1 (Chlorophyll)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.- (Oxidoreductases)
RN  - EC 1.13.- (Oxygenases)
RN  - EC 1.13.- (pheide a oxygenase)
RN  - EC 1.14.13.39 (NOA1 protein, Arabidopsis)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.3.7.- (ACD2 protein, Arabidopsis)
RN  - IA2WNI2HO2 (pheophorbide a)
SB  - IM
MH  - Apoptosis Regulatory Proteins/genetics/metabolism
MH  - Arabidopsis/genetics/*metabolism/radiation effects
MH  - Arabidopsis Proteins/genetics/metabolism
MH  - Blotting, Western
MH  - Chlorophyll/analogs & derivatives/*metabolism
MH  - Chloroplasts/metabolism/radiation effects/ultrastructure
MH  - Darkness
MH  - Gene Expression Regulation, Enzymologic/radiation effects
MH  - Gene Expression Regulation, Plant/radiation effects
MH  - Microscopy, Electron, Transmission
MH  - Mutation
MH  - Nitric Oxide/*metabolism
MH  - Nitric Oxide Synthase/genetics/metabolism
MH  - Oxidoreductases/genetics/metabolism
MH  - Oxygenases/genetics/metabolism
MH  - Photosynthesis/genetics/radiation effects
MH  - Plant Leaves/genetics/*metabolism/radiation effects
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Thylakoids/*metabolism/radiation effects
MH  - Time Factors
PMC - PMC3572010
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/02/19 06:00
MHDA- 2013/08/28 06:00
PMCR- 2013/02/13
CRDT- 2013/02/19 06:00
PHST- 2012/09/25 00:00 [received]
PHST- 2013/01/08 00:00 [accepted]
PHST- 2013/02/19 06:00 [entrez]
PHST- 2013/02/19 06:00 [pubmed]
PHST- 2013/08/28 06:00 [medline]
PHST- 2013/02/13 00:00 [pmc-release]
AID - PONE-D-12-29094 [pii]
AID - 10.1371/journal.pone.0056345 [doi]
PST - ppublish
SO  - PLoS One. 2013;8(2):e56345. doi: 10.1371/journal.pone.0056345. Epub 2013 Feb 13.