Mutation of Arabidopsis BARD1 causes meristem defects by failing to confine WUSCHEL expression to the organizing center
Mutation of Arabidopsis BARD1 causes meristem defects by failing to confine WUSCHEL expression to the organizing center
复制标题
拟南芥 BARD1 突变无法将 WUSCHEL 表达限制在组织中心，从而导致分生组织缺陷
DOI：
10.1105/tpc.108.058867
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发表时间：
2008-06-01
期刊：
影响因子：
11.6
通讯作者：
Zhu, Yu-Xian
中科院分区：
文献类型：
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作者：
Han, Pei;Li, Qing;Zhu, Yu-Xian
拟南芥芽的顶端分生组织（SAM）中的干细胞命运由Wuschel（WUS）和Clavata控制。在这里，我们检查了BARD1（对于BRCA1相关的环域1），以前与DNA修复功能有关。我们发现它还调节WUS表达。我们观察到敲除突变体Bard1-3中的SAM缺陷。与野生型相比，在Bard1-3中积累的WUS转录本在Bard1-3中累积> 238倍，主要位于最外层的细胞层而不是通常的组织中心。通过从野生型植物获得的核蛋白提取物识别出特定的WUS启动子区域，并且该蛋白-DNA复合物通过抗Bard1的抗体识别。双突变体（WUS-1 BARD1-3）表现出与WUS-1相同的过早终止的SAM结构，表明BARD1通过调节WUS的功能。 Bard1的过表达导致WUS转录水平降低，从而产生了WUS-1样表型。全长bard1或编码C末端结构域（Bard1：c-ter; Bard1-3）的克隆足以补充Bard1-3表型，表明BARD1通过其C末端域功能。我们的数据表明，Bard1通过将WUS表达限制为组织中心来调节SAM组织和维护。
Stem cell fate in the Arabidopsis thaliana shoot apical meristem (SAM) is controlled by WUSCHEL (WUS) and CLAVATA. Here, we examine BARD1 (for BRCA1-associated RING domain 1), which had previously been implicated in DNA repair functions; we find that it also regulates WUS expression. We observed severe SAM defects in the knockout mutant bard1-3. WUS transcripts accumulated > 238-fold in bard1-3 compared with the wild type and were located mainly in the outermost cell layers instead of the usual organizing center. A specific WUS promoter region was recognized by nuclear protein extracts obtained from wild-type plants, and this protein-DNA complex was recognized by antibodies against BARD1. The double mutant (wus-1 bard1-3) showed prematurely terminated SAM structures identical to those of wus-1, indicating that BARD1 functions through regulation of WUS. BARD1 overexpression resulted in reduced WUS transcript levels, giving a wus-1-like phenotype. Either full-length BARD1 or a clone that encoded the C-terminal domain (BARD1: C-ter;bard1-3) was sufficient to complement the bard1-3 phenotype, indicating that BARD1 functions through its C-terminal domain. Our data suggest that BARD1 regulates SAM organization and maintenance by limiting WUS expression to the organizing center.