AtLa1 protein initiates IRES-dependent translation of WUSCHEL mRNA and regulates the stem cell homeostasis of Arabidopsis in response to environmental hazards
AtLa1 protein initiates IRES-dependent translation of WUSCHEL mRNA and regulates the stem cell homeostasis of Arabidopsis in response to environmental hazards
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DOI：
10.1111/pce.12535
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发表时间：
2015-10-01
影响因子：
7.3
通讯作者：
Huang, Tao
中科院分区：
文献类型：
--
作者：
Cui, Yuchao;Rao, Shaofei;Huang, Tao
植物干细胞在其整个生命周期中对环境危害高度敏感，但植物保护干细胞稳态以应对环境危害的机制在很大程度上是未知的。同源结构域转录因子WUSCHEL（WUS）蛋白维持拟南芥茎顶端分生组织中的干细胞库。在这里，我们证明了WUS mRNA的翻译是由位于5 '-非翻译区的内部核糖体进入位点（IRES）指导的。AtLa 1蛋白是一种RNA结合因子，与5 '-非翻译区结合并启动WUS mRNA的IRES依赖性翻译。AtLa 1表达的敲低抑制了WUS IRES依赖的翻译，并导致生长和发育的停滞。AtLa 1蛋白主要定位于核质中。然而，环境危害促进了AtLa 1蛋白的核质易位，这进一步增强了WUS mRNA的IRES依赖性翻译。遗传证据表明，WUS蛋白增加了茎尖分生组织对环境危害的耐受性。基于这些结果，我们得出结论，拟南芥中的干细胞生态位通过增强AtLa 1蛋白控制下的WUS mRNA的IRES依赖性翻译来应对环境危害。
Plant stem cells are hypersensitive to environmental hazards throughout their life cycle, but the mechanism by which plants safeguard stem cell homeostasis in response to environmental hazards is largely unknown. The homeodomain transcription factor WUSCHEL (WUS) protein maintains the stem cell pool in the shoot apical meristem of Arabidopsis. Here, we demonstrate that the translation of WUS mRNA is directed by an internal ribosomal entry site (IRES) located in the 5'-untranslated region. The AtLa1 protein, an RNA-binding factor, binds to the 5'-untranslated region and initiates the IRES-dependent translation of WUS mRNA. Knockdown of AtLa1 expression represses the WUS IRES-dependent translation and leads to the arrest of growth and development. The AtLa1 protein is mainly located in the nucleoplasm. However, environmental hazards promote the nuclear-to-cytoplasmic translocation of the AtLa1 protein, which further enhances the IRES-dependent translation of WUS mRNA. Genetic evidence indicates that the WUS protein increases the tolerance of the shoot apical meristem to environmental hazards. Based on these results, we conclude that the stem cell niche in Arabidopsis copes with environmental hazards by enhancing the IRES-dependent translation of WUS mRNA under the control of the AtLa1 protein.