The AP2/ERF Transcription Factor WIND1 Controls Cell Dedifferentiation in Arabidopsis
The AP2/ERF Transcription Factor WIND1 Controls Cell Dedifferentiation in Arabidopsis
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DOI：
10.1016/j.cub.2011.02.020
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发表时间：
2011-03-22
期刊：
影响因子：
9.2
通讯作者：
Ohme-Takagi, Masaru
中科院分区：
文献类型：
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作者：
Iwase, Akira;Mitsuda, Nobutaka;Ohme-Takagi, Masaru
许多多细胞生物在受伤后具有再生新器官的显著能力。作为器官再生的第一步，成年体细胞通常去分化以重新获得细胞增殖潜力，但这一过程的机制在植物中仍然未知。在这里，我们表明，AP 2/ERF转录因子，伤口诱导的去分化1（WIND 1），参与控制细胞的拟南芥去分化。WIND 1在伤口部位被快速诱导，并且它促进细胞去分化和随后的细胞增殖以形成称为愈伤组织的多能细胞团。我们进一步证明，WIND 1的异位过表达足以在没有外源生长素和细胞分裂素的情况下建立和维持体细胞的去分化状态，这两种植物激素通常是细胞去分化所需的[1]。合成细胞分裂素报告基因的体内成像[2]揭示，创伤上调B型拟南芥反应调节因子（ARR）介导的细胞分裂素反应，WIND 1通过ARR依赖性信号通路起作用，促进细胞去分化。这项研究提供了新的分子见解，植物如何控制细胞去分化响应创伤。
Many multicellular organisms have remarkable capability to regenerate new organs after wounding. As a first step of organ regeneration, adult somatic cells often dedifferentiate to reacquire cell proliferation potential, but mechanisms underlying this process remain unknown in plants. Here we show that an AP2/ERF transcription factor, WOUND INDUCED DEDIFFERENTIATION 1 (WIND1), is involved in the control of cell dedifferentiation in Arabidopsis. WIND1 is rapidly induced at the wound site, and it promotes cell dedifferentiation and subsequent cell proliferation to form a mass of pluripotent cells termed callus. We further demonstrate that ectopic overexpression of WIND1 is sufficient to establish and maintain the dedifferentiated status of somatic cells without exogenous auxin and cytokinin, two plant hormones that are normally required for cell dedifferentiation [1]. In vivo imaging of a synthetic cytokinin reporter [2] reveals that wounding upregulates the B-type ARABIDOPSIS RESPONSE REGULATOR (ARR)-mediated cytokinin response and that WIND1 acts via the ARR-dependent signaling pathway to promote cell dedifferentiation. This study provides novel molecular insights into how plants control cell dedifferentiation in response to wounding.