A mutation in the Arabidopsis mTERF-related plastid protein SOLDAT10 activates retrograde signaling and suppresses 1O2-induced cell death
A mutation in the Arabidopsis mTERF-related plastid protein SOLDAT10 activates retrograde signaling and suppresses 1O2-induced cell death
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DOI：
10.1111/j.1365-313x.2009.03965.x
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发表时间：
2009-11-01
期刊：
影响因子：
7.2
通讯作者：
Apel, Klaus
中科院分区：
文献类型：
--
作者：
Meskauskiene, Rasa;Wuersch, Marco;Apel, Klaus
拟南芥的条件流感突变体在从暗到光的转变过程中产生单线态氧（10o(2)）。流感的幼苗会漂白并死亡，而成熟的植物会停止生长并形成肉眼可见的坏死性损伤。几个抑制突变体，被称为单线态氧联死亡激活因子（soldat），被确定为废除10(2)介导的流感幼苗细胞死亡。其中一个soldat突变，soldat10，影响一个编码与人类线粒体转录终止因子mTERF相关的质体定位蛋白的基因。由于这种突变，soldat10的质体特异性rRNA水平降低，蛋白质合成减弱。这种对幼苗叶绿体稳态的破坏影响了叶绿体与细胞核之间的交流，并导致核基因转录物的稳态浓度发生变化。胁迫相关基因的组成性上调表明，紫苏幼苗遭受轻度光氧化胁迫。即使幼苗在黑暗中过度积累光敏剂原叶绿内酯，并在从暗到光的转变后激活10o(2)响应基因的表达，它们也不会表现出10o(2)依赖的细胞死亡反应。在新出现的植物/流感幼苗中，叶绿体稳态的紊乱似乎可以拮抗随后的o(2)介导的细胞死亡反应，而不会抑制o(2)依赖的逆行信号。这项工作的结果揭示了通常被称为“质体信号”的意想不到的复杂性。
P>The conditional flu mutant of Arabidopsis thaliana generates singlet oxygen (1O(2)) in plastids during a dark-to-light shift. Seedlings of flu bleach and die, whereas mature plants stop growing and develop macroscopic necrotic lesions. Several suppressor mutants, dubbed singlet oxygen-linked death activator (soldat), were identified that abrogate 1O(2)-mediated cell death of flu seedlings. One of the soldat mutations, soldat10, affects a gene encoding a plastid-localized protein related to the human mitochondrial transcription termination factor mTERF. As a consequence of this mutation, plastid-specific rRNA levels decrease and protein synthesis in plastids of soldat10 is attenuated. This disruption of chloroplast homeostasis in soldat10 seedlings affects communication between chloroplasts and the nucleus and leads to changes in the steady-state concentration of nuclear gene transcripts. The soldat10 seedlings suffer from mild photo-oxidative stress, as indicated by the constitutive up-regulation of stress-related genes. Even though soldat10/flu seedlings overaccumulate the photosensitizer protochlorophyllide in the dark and activate the expression of 1O(2)-responsive genes after a dark-to-light shift they do not show a 1O(2)-dependent cell death response. Disturbance of chloroplast homeostasis in emerging soldat10/flu seedlings seems to antagonize a subsequent 1O(2)-mediated cell death response without suppressing 1O(2)-dependent retrograde signaling. The results of this work reveal the unexpected complexity of what is commonly referred to as 'plastid signaling'.