Lee Il Hwan, Lee In Chul, Kim Jeongsik, Kim Jin Hee, Chung Eui-Hwan, Kim Hyo Jung, Park Su Jin, Kim Yong Min, Kang Sin Kyu, Nam Hong Gil, Woo Hye Ryun, Lim Pyung Ok
Department of Life Sciences, POSTECH, Pohang, 37673, Republic of Korea.
Center for Plant Aging Research, Institute for Basic Science (IBS), Daegu, 42988, Republic of Korea.
Physiol Plant. 2016 Oct;158(2):180-99. doi: 10.1111/ppl.12434. Epub 2016 Jun 1.
Leaf senescence is not only primarily governed by developmental age but also influenced by various internal and external factors. Although some genes that control leaf senescence have been identified, the detailed regulatory mechanisms underlying integration of diverse senescence-associated signals into the senescence programs remain to be elucidated. To dissect the regulatory pathways involved in leaf senescence, we isolated the not oresara1-1 (nore1-1) mutant showing accelerated leaf senescence phenotypes from an EMS-mutagenized Arabidopsis thaliana population. We found that altered transcriptional programs in defense response-related processes were associated with the accelerated leaf senescence phenotypes observed in nore1-1 through microarray analysis. The nore1-1 mutation activated defense program, leading to enhanced disease resistance. Intriguingly, high ambient temperature effectively suppresses the early senescence and death phenotypes of nore1-1. The gene responsible for the phenotypes of nore1-1 contains a missense mutation in SENESCENCE-ASSOCIATED E3 UBIQUITIN LIGASE 1 (SAUL1), which was reported as a negative regulator of premature senescence in the light intensity- and PHYTOALEXIN DEFICIENT 4 (PAD4)-dependent manner. Through extensive double mutant analyses, we recently identified suppressor of the G2 Allele of SKP1b (SGT1b), one of the positive regulators for disease resistance conferred by many resistance (R) proteins, as a downstream signaling component in NORE1-mediated senescence and cell death pathways. In conclusion, NORE1/SAUL1 is a key factor integrating signals from temperature-dependent defense programs and leaf senescence in Arabidopsis. These findings provide a new insight that plants might utilize defense response program in regulating leaf senescence process, possibly through recruiting the related genes during the evolution of the leaf senescence program.
叶片衰老不仅主要受发育年龄的调控，还受到各种内部和外部因素的影响。尽管已经鉴定出一些控制叶片衰老的基因，但将多种衰老相关信号整合到衰老程序中的详细调控机制仍有待阐明。为了剖析参与叶片衰老的调控途径，我们从经甲基磺酸乙酯（EMS）诱变的拟南芥群体中分离出了具有加速叶片衰老表型的not oresara1-1（nore1-1）突变体。通过微阵列分析，我们发现与防御反应相关过程中改变的转录程序与在nore1-1中观察到的加速叶片衰老表型有关。nore1-1突变激活了防御程序，导致抗病性增强。有趣的是，高环境温度能有效抑制nore1-1的早期衰老和死亡表型。导致nore1-1表型的基因在衰老相关E3泛素连接酶1（SAUL1）中存在一个错义突变，SAUL1被报道为以光强度和植物抗毒素缺陷4（PAD4）依赖的方式负调控早衰。通过广泛的双突变分析，我们最近鉴定出SKP1b的G2等位基因的抑制子（SGT1b），它是许多抗性（R）蛋白赋予抗病性的正调控因子之一，是NORE1介导的衰老和细胞死亡途径中的下游信号成分。总之，NORE1/SAUL1是整合来自拟南芥温度依赖防御程序和叶片衰老信号的关键因子。这些发现提供了一个新的见解，即植物可能利用防御反应程序来调控叶片衰老过程，可能是通过在叶片衰老程序的进化过程中招募相关基因来实现的。
