Hypersensitivity to DNA damage in plant stem cell niches
Hypersensitivity to DNA damage in plant stem cell niches
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DOI：
10.1073/pnas.0909218106
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发表时间：
2009-12-08
影响因子：
11.1
通讯作者：
Sablowski, Robert
中科院分区：
文献类型：
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作者：
Fulcher, Nick;Sablowski, Robert
植物生长的顶端含有不断产生组织的干细胞，在芽中，包括生殖细胞。这些干细胞群体在植物的整个生命周期中保持活跃，可以持续几个世纪，并且特别暴露于导致DNA损伤和突变的环境危害。目前还不知道植物是否有机制来保护这些关键细胞群中的基因组。在这里，我们表明，根和芽干细胞和它们的早期后代被选择性地杀死温和的治疗与拟放射性药物，X射线，或突变，破坏DNA修复的非同源末端连接。干细胞死亡需要通过共济失调-毛细血管扩张突变（ATM）激酶以及（特别是在根中）ATM/RAD 3相关（ATR）激酶转导DNA损伤信号。与植物中p53和核心凋亡机制的缺乏一致，干细胞的死亡没有显示出凋亡，而是自溶特征，如在植物发育程序性细胞死亡的其他情况下所见。我们认为，植物已经独立地进化出选择性死亡作为一种严格的机制，以保障其干细胞群体的基因组完整性。
The growing apices of plants contain stem cells that continually produce tissues, which, in the shoot, include the germline. These stem cell populations remain active throughout the plant's life, which can last for centuries, and are particularly exposed to environmental hazards that cause DNA damage and mutations. It is not known whether plants have mechanisms to safeguard the genome specifically in these crucial cell populations. Here, we show that root and shoot stem cells and their early descendants are selectively killed by mild treatment with radiomimetic drugs, x-rays, or mutations that disrupt DNA repair by nonhomologous end-joining. Stem cell death required transduction of DNA damage signals by the ATAXIA-TELANGIECTASIA MUTATED (ATM) kinase and, specifically in the root, also the ATM/RAD3-RELATED (ATR) kinase. Consistent with the absence of p53 and the core apoptotic machinery in plants, death of the stem cells did not show apoptotic but autolytic features as seen in other cases of plant developmentally programmed cell death. We propose that plants have independently evolved selective death as a stringent mechanism to safeguard genome integrity in their stem cell populations.