Accelerated cell death 2 suppresses mitochondrial oxidative bursts and modulates cell death in Arabidopsis.
Accelerated cell death 2 suppresses mitochondrial oxidative bursts and modulates cell death in Arabidopsis.
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DOI：
10.1111/j.1365-313x.2011.04814.x
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发表时间：
2012-02
期刊：
影响因子：
--
通讯作者：
Greenberg JT
中科院分区：
文献类型：
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作者：
Pattanayak GK;Venkataramani S;Hortensteiner S;Kunz L;Christ B;Moulin M;Smith AG;Okamoto Y;Tamiaki H;Sugishima M;Greenberg JT
拟南芥加速细胞死亡2 （ACD2）蛋白保护细胞免受内源性卟啉相关分子如红色叶绿素分解代谢物或外源性原卟啉IX引起的程序性细胞死亡（PCD）。我们之前发现，在细菌感染过程中，叶绿素分解酶ACD2定位于叶片的叶绿体和线粒体。此外，acd2细胞表现出线粒体功能障碍。在具有acd2和acd2 +部门的植物中，acd2具有细胞自主功能，这意味着促死亡的acd2底物在促进PCD扩散中具有细胞非自主性。单独靶向线粒体的ACD2可以减少起源于叶绿体的ACD2底物的积累，这表明ACD2底物分子可能在细胞内移动。线粒体中两种不同的光依赖性活性氧爆发在acd2 PCD表型中起着突出的因果作用。最后，只要ACD2具有催化活性，就可以分别靶向线粒体或叶绿体，与ACD2互补；结合底物的能力不足以使ACD2在体内或体外发挥作用。综上所述，这些数据表明，ACD2在感染过程中动态定位，以保护细胞免受促死亡移动底物分子的侵害，其中一些底物可能起源于叶绿体，但对线粒体有主要影响。
The Arabidopsis ACCELERATED CELL DEATH 2 (ACD2) protein protects cells from programmed cell death (PCD) caused by endogenous porphyrin-related molecules like red chlorophyll catabolite or exogenous protoporphyrin IX. We previously found that during bacterial infection, ACD2, a chlorophyll breakdown enzyme, localizes to both chloroplasts and mitochondria in leaves. Additionally, acd2 cells show mitochondrial dysfunctions. In plants with acd2 and ACD2+ sectors, ACD2 functions cell autonomously, implicating a pro-death ACD2 substrate as cell non-autonomous in promoting spreading PCD. ACD2 targeted solely to mitochondria can reduce the accumulation of an ACD2 substrate that originates in chloroplasts, indicating that ACD2 substrate molecules are likely mobile within cells. Two different light-dependent reactive oxygen bursts in mitochondria play prominent and causal roles in the acd2 PCD phenotype. Finally, ACD2 can complement acd2 when targeted to mitochondria or chloroplasts, respectively, as long as it is catalytically active; the ability to bind substrate is not sufficient for ACD2 to function in vitro or in vivo. Together the data suggest that ACD2 localizes dynamically during infection to protect cells from pro-death mobile substrate molecules, some of which may originate in chloroplasts, but have major effects on mitochondria.