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, the Chinese Academy of Sciences, Shanghai 200032, China.
J Integr Plant Biol. 2012 Aug;54(8):516-25. doi: 10.1111/j.1744-7909.2012.01140.x.
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.
一氧化氮（NO）缺乏突变体 nos1/noa1 表现出早期叶片衰老表型。乙烯不敏感 2（EIN2）先前被报道作为乙烯诱导衰老的正调节剂。本研究旨在通过表征双突变体 ein2-1 nos1/noa1（拟南芥）来解决 NO 如何与乙烯相互作用调节叶片衰老的问题。双突变体分析表明，EIN2 突变抑制了 nos1/noa1 介导的黑暗诱导的早期衰老表型，表明 EIN2 参与 NO 信号在叶片衰老调控中的作用。结果表明，在双突变体叶片中，叶绿素降解明显延迟。此外，EIN2 突变逆转了 nos1/noa1 介导的光化学效率和类囊体膜完整性的损害。在叶片衰老过程中，nos1/noa1 突变体中快速上调的已知衰老标记基因的表达在双突变体中受到严重抑制。有趣的是，黑暗生长的 nos1/noa1 突变体幼苗对乙烯的反应与野生型幼苗相似。综上所述，我们的研究结果表明，EIN2 参与由 NO 缺乏引起的早期叶片衰老的调控，但 NOS1/NOA1 突变引起的 NO 缺乏不影响乙烯信号。
