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Nitric Oxide Regulates Dark‐Induced Leaf Senescence Through EIN2 in Arabidopsis F
Author(s) -
Niu YunHan,
Guo FangQing
Publication year - 2012
Publication title -
journal of integrative plant biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.734
H-Index - 83
eISSN - 1744-7909
pISSN - 1672-9072
DOI - 10.1111/j.1744-7909.2012.01140.x
Subject(s) - senescence , mutant , nitric oxide , microbiology and biotechnology , arabidopsis , nos1 , biology , phenotype , arabidopsis thaliana , biochemistry , nitric oxide synthase , gene , endocrinology
Abstract The nitric oxide (NO)‐deficient mutant nos1/noa1 exhibited an early leaf senescence phenotype. ETHYLENE INSENSITIVE 2 ( EIN2 ) was previously reported to function as a positive regulator of ethylene‐induced senescence. The aim of this study was to address the question of how NO interacts with ethylene to regulate leaf senescence by characterizing the double mutant ein2‐1 nos1/noa1 ( Arabidopsis thaliana ). Double mutant analysis revealed that the nos1/noa1 ‐mediated, dark‐induced early senescence phenotype was suppressed by mutations in EIN2 , suggesting that EIN2 is involved in nitric oxide signaling in the regulation of leaf senescence. The results showed that chlorophyll degradation in the double mutant leaves was significantly delayed. In addition, nos1/noa1 ‐mediated impairment in photochemical efficiency and integrity of thylakoid membranes was reverted by EIN2 mutations. The rapid upregulation of the known senescence marker genes in the nos1/noa1 mutant was severely inhibited in the double mutant during leaf senescence. Interestingly, the response of dark‐grown nos1/noa1 mutant seedlings to ethylene was similar to that of wild type seedlings. Taken together, our findings suggest that EIN2 is involved in the regulation of early leaf senescence caused by NO deficiency, but NO deficiency caused by NOS1/NOA1 mutations does not affect ethylene signaling .