A Two-Step Model for de Novo Activation of WUSCHEL during Plant Shoot Regeneration

A Two-Step Model for de Novo Activation of WUSCHEL during Plant Shoot Regeneration
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植物芽再生过程中 WUSCHEL 从头激活的两步模型

DOI:
10.1105/tpc.16.00863
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发表时间:
2017-04
期刊:
影响因子:
11.6
通讯作者:
Wang Jia Wei
Wang Jia Wei
中科院分区:
生物学1区
文献类型:
--
作者:
Zhang Tian Qi;Lian Heng;Zhou Chuan Miao;Xu Lin;Jiao Yuling;Wang Jia Wei

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在富含细胞分裂素的环境中,抑制性组蛋白标记的去除引发了B型拟南芥应答调节因子和HD-ZIP III转录因子对WUSCHEL的重新激活。植物细胞是全能的,能够从分化的器官再生。60年来,人们已经知道富含细胞分裂素的培养基诱导愈伤组织细胞再生芽。然而,潜在的分子机制仍然难以捉摸。同源结构域转录因子WUSCHEL(WUS)是拟南芥茎干细胞生态位从头建立所必需的。我们发现,WUS阳性(WUS+)细胞标记再生过程中的芽祖细胞区域。富含细胞分裂素的环境最初以细胞周期依赖性的方式促进WUS基因座上抑制性组蛋白标记H3 K27 me 3的去除。随后,在细胞分裂素信号通路中作为转录激活因子发挥作用的B型拟南芥应答调节因子(ARR)ARR 1、ARR 2、ARR 10和ARR 12通过与microRNA 165/6靶向的HD-ZIP III转录因子结合,在空间上激活WUS表达。因此,我们的研究结果提供了重要的见解细胞分裂素指导的芽再生的分子框架,并揭示了一个两步机制从头激活WUS。
The removal of repressive histone marks in a cytokinin-rich environment primes de novo activation of WUSCHEL by B-type ARABIDOPSIS RESPONSE REGULATORs and HD-ZIP III transcription factors. Plant cells are totipotent and competent to regenerate from differentiated organs. It has been known for six decades that cytokinin-rich medium induces shoot regeneration from callus cells. However, the underlying molecular mechanism remains elusive. The homeodomain transcription factor WUSCHEL (WUS) is essential for de novo establishment of the shoot stem cell niche in Arabidopsis thaliana. We found that WUS-positive (WUS+) cells mark the shoot progenitor region during regeneration. A cytokinin-rich environment initially promotes the removal of the repressive histone mark H3K27me3 at the WUS locus in a cell cycle-dependent manner. Subsequently, the B-type ARABIDOPSIS RESPONSE REGULATORs (ARRs) ARR1, ARR2, ARR10, and ARR12, which function as transcriptional activators in the cytokinin signaling pathway, spatially activate WUS expression through binding with microRNA165/6-targeted HD-ZIP III transcription factors. Thus, our results provide important insights into the molecular framework for cytokinin-directed shoot regeneration and reveal a two-step mechanism for de novo activation of WUS.
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