How a retrotransposon exploits the plant's heat stress response for its activation.
How a retrotransposon exploits the plant's heat stress response for its activation.
复制标题
DOI：
10.1371/journal.pgen.1004115
复制
发表时间：
2014-01
期刊：
影响因子：
4.5
通讯作者：
Mittelsten Scheid O
中科院分区：
文献类型：
--
作者：
Cavrak VV;Lettner N;Jamge S;Kosarewicz A;Bayer LM;Mittelsten Scheid O
反转录转座子是动植物基因组的主要组成部分。它们通过逆转录扩增并重新整合到宿主基因组中，但它们的活性通常在表观遗传学上沉默。在植物中，逆转录转座子的基因组拷贝通常与通过RNA指导的DNA甲基化安装和维持的抑制性染色质修饰相关。为了逃避这种严格的控制，反转录转座子采用各种策略来避免表观遗传沉默。在这里，我们描述了ONSEN，LTR-copia型逆转录转座子在拟南芥中开发的机制。ONSEN获得了一种被植物来源的热应激防御因子识别的热响应元件，导致在高温下转录和产生全长染色体外DNA。此外，ONSEN启动子不含CG和CHG位点，并且CHH位点处DNA甲基化的降低不足以激活该元件。由于分裂细胞具有更明显的热反应，能够重新整合到基因组中的染色体外ONSEN DNA优先积累在芽的分生组织中。在热胁迫期间，主要植物热激转录因子的募集利用植物的热胁迫反应来实现转座子的激活，使得宿主不可能在不失去对入侵者的控制的情况下对胁迫做出适当的反应。转座子被编程为在其宿主基因组内扩增。在防御中，宿主已经进化出阻止转座子激活的机制，通常是通过表观遗传转录沉默。宿主和入侵者之间持续不断的、可能无休止的军备竞赛带来了不同的策略，以相互抵消对方的诡计。几种这样的策略组合在拟南芥基因组中的一个转座子中。其启动子缺乏稳定维持抑制性DNA甲基化所必需的对称位点，并且在剩余胞嘧啶处甲基化的减少不会激活该元件。更复杂的是：其启动子与热胁迫响应植物基因共享一个序列基序，并被热诱导植物转录因子识别。当植物必须在高温下激活其热应激防御时，转座子能够产生新的染色体外DNA拷贝，这些拷贝可以潜在地整合到基因组的新位点中。此外，热反应在具有分裂细胞的组织中特别强，其因此形成最大量的染色体外转座子拷贝。我们认为这是“披着羊皮的狼”策略的一个例子，即转座子只有在宿主的特定压力条件下才能被看到。
Retrotransposons are major components of plant and animal genomes. They amplify by reverse transcription and reintegration into the host genome but their activity is usually epigenetically silenced. In plants, genomic copies of retrotransposons are typically associated with repressive chromatin modifications installed and maintained by RNA-directed DNA methylation. To escape this tight control, retrotransposons employ various strategies to avoid epigenetic silencing. Here we describe the mechanism developed by ONSEN, an LTR-copia type retrotransposon in Arabidopsis thaliana. ONSEN has acquired a heat-responsive element recognized by plant-derived heat stress defense factors, resulting in transcription and production of full length extrachromosomal DNA under elevated temperatures. Further, the ONSEN promoter is free of CG and CHG sites, and the reduction of DNA methylation at the CHH sites is not sufficient to activate the element. Since dividing cells have a more pronounced heat response, the extrachromosomal ONSEN DNA, capable of reintegrating into the genome, accumulates preferentially in the meristematic tissue of the shoot. The recruitment of a major plant heat shock transcription factor in periods of heat stress exploits the plant's heat stress response to achieve the transposon's activation, making it impossible for the host to respond appropriately to stress without losing control over the invader. Transposons are programmed to amplify within their host genomes. In defense, hosts have evolved mechanisms to impede transposon activation, often by epigenetic transcriptional silencing. A constant and likely unending arms race between host and invader has brought about different strategies to mutually counteract the tricks of the other. Several such strategies are combined in one transposon in the Arabidopsis genome. Its promoter is devoid of symmetric sites necessary for stable maintenance of repressive DNA methylation, and a reduction of methylation at the remaining cytosines does not activate the element. More sophisticated still: its promoter shares a sequence motif with heat stress-responsive plant genes and is recognized by a heat-induced plant transcription factor. Whenever the plants must activate their heat stress defense under high temperatures, the transposon is able to generate new extrachromosomal DNA copies that can potentially integrate into new sites of the genome. In addition, the heat response is especially strong in tissue with dividing cells, which form consequently the largest amount of extrachromosomal transposon copies. We see this as an example of a “wolf in sheep's clothing” strategy, whereby the transposon becomes visible as such only under specific stress conditions of its host.
登录
查看更多内容
影响因子：
64.8
作者：
Ito, Hidetaka;Gaubert, Herve;Paszkowski, Jerzy
通讯作者：
Paszkowski, Jerzy
影响因子：
8.3
作者：
De Felice B;Wilson RR;Argenziano C;Kafantaris I;Conicella C
通讯作者：
Conicella C
影响因子：
7.2
作者：
Clough, SJ;Bent, AF
通讯作者：
Bent, AF
影响因子：
64.8
作者：
Jackson, JP;Lindroth, AM;Jacobsen, SE
通讯作者：
Jacobsen, SE
影响因子：
5.4
作者：
Feuerbach, F;Drouaud, J;Lucas, H
通讯作者：
Lucas, H