Expression of a dominant‐negative AtNEET‐H89C protein disrupts iron–sulfur metabolism and iron homeostasis in Arabidopsis
Expression of a dominant‐negative AtNEET‐H89C protein disrupts iron–sulfur metabolism and iron homeostasis in Arabidopsis
复制标题
拟南芥中显性负性 AtNEET-H89C 蛋白的表达会破坏铁硫代谢和铁稳态
DOI：
10.1111/tpj.14581
复制
发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Mendoza‐Cozatl, David G.
中科院分区：
文献类型：
--
作者：
Zandalinas, Sara I.;Song, Luhua;Sengupta, Soham;McInturf, Samuel A.;Grant, DeAna G.;Marjault, Henri‐Baptiste;Castro‐Guerrero, Norma A.;Burks, David;Azad, Rajeev K.;Mendoza‐Cozatl, David G.
铁硫（Fe-S）簇作为介导多种电子转移反应的蛋白质辅助因子在植物中发挥着重要作用。由于它们可以与氧反应形成活性氧（ROS）并造成细胞损伤，因此 Fe-S 簇的生物发生受到高度调控。最近发现的一组 2Fe-2S 蛋白（称为 NEET 蛋白）被提议协调哺乳动物细胞中的 Fe-S、Fe 和 ROS 稳态。在此，我们报道，破坏拟南芥 NEET 蛋白家族唯一成员 AtNEET 的功能，会引发叶片相关的 Fe-S 和 Fe 缺乏反应、叶绿体中 Fe 含量升高（1.2-1.5 倍）、失绿、叶绿体结构损伤和高幼苗死亡率。我们的研究结果表明，破坏AtNEET功能会破坏2Fe-2S簇从叶绿体2Fe-2S生物发生途径向不同细胞质和叶绿体Fe-S蛋白以及细胞质Fe-S生物发生系统的转移，并且解偶联这一过程会触发叶片相关的Fe-S和Fe缺乏反应，导致叶绿体中Fe过度积累并增强ROS积累。我们进一步表明，AtNEET 将其 2Fe-2S 簇转移到 DRE2（细胞质 Fe-S 生物发生系统的关键蛋白），并提出叶绿体和细胞质中 2Fe-2S 簇的可用性与植物中的 Fe 稳态有关。
Iron–sulfur (Fe–S) clusters play an essential role in plants as protein cofactors mediating diverse electron transfer reactions. Because they can react with oxygen to form reactive oxygen species (ROS) and inflict cellular damage, the biogenesis of Fe–S clusters is highly regulated. A recently discovered group of 2Fe–2S proteins, termed NEET proteins, was proposed to coordinate Fe–S, Fe and ROS homeostasis in mammalian cells. Here we report that disrupting the function of AtNEET, the sole member of the NEET protein family inArabidopsis thaliana, triggers leaf‐associated Fe–S‐ and Fe‐deficiency responses, elevated Fe content in chloroplasts (1.2–1.5‐fold), chlorosis, structural damage to chloroplasts and a high seedling mortality rate. Our findings suggest that disrupting AtNEET function disrupts the transfer of 2Fe–2S clusters from the chloroplastic 2Fe–2S biogenesis pathway to different cytosolic and chloroplastic Fe–S proteins, as well as to the cytosolic Fe–S biogenesis system, and that uncoupling this process triggers leaf‐associated Fe–S‐ and Fe‐deficiency responses that result in Fe over‐accumulation in chloroplasts and enhanced ROS accumulation. We further show that AtNEET transfers its 2Fe–2S clusters to DRE2, a key protein of the cytosolic Fe–S biogenesis system, and propose that the availability of 2Fe–2S clusters in the chloroplast and cytosol is linked to Fe homeostasis in plants.