RopGEF7 Regulates PLETHORA-Dependent Maintenance of the Root Stem Cell Niche in Arabidopsis

RopGEF7 Regulates PLETHORA-Dependent Maintenance of the Root Stem Cell Niche in Arabidopsis
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DOI:
10.1105/tpc.111.085514
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发表时间:
2011-08-01
期刊:
影响因子:
11.6
通讯作者:
Tao, Li-zhen
Tao, Li-zhen
中科院分区:
生物学1区
文献类型:
--
作者:
Chen, Min;Liu, Huili;Tao, Li-zhen

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根干细胞龛定义了指定和维持干细胞的区域,并且对于维持根生长至关重要。在这里,我们的特点和研究的功能作用的静止中心(QC)表达RAC/ROP GTd 3激活剂,RopGEF 7,在拟南芥。我们发现,RopGEF 7与RAC 1相互作用,C-末端截短的组成型活性RopGEF 7(RopGEF 7 DC)的过表达激活RAC/ROP GTP酶。通过RNA干扰敲低RopGEF 7导致胚胎图案形成和QC维持的缺陷,并导致根干细胞群体的胚后损失。基因表达研究表明,RopGEF 7是根分生组织维持所必需的,因为它调节PLETHORA 1(PLT 1)和PLT 2的表达,这是介导根干细胞生态位模式的关键转录因子。遗传分析表明RopGEF 7与PLT基因相互作用以调节QC维持。此外,RopGEF 7是由生长素诱导的转录,而其功能是生长素流出蛋白PIN 1的表达和胚和幼苗根中正常生长素最大值的维持所需的。这些结果表明,RopGEF 7可以整合生长素衍生的位置信息的前馈机制,调节PLT转录因子,从而控制根干细胞龛的维护。
The root stem cell niche defines the area that specifies and maintains the stem cells and is essential for the maintenance of root growth. Here, we characterize and examine the functional role of a quiescent center (QC)-expressed RAC/ROP GTPase activator, RopGEF7, in Arabidopsis thaliana. We show that RopGEF7 interacts with At RAC1 and overexpression of a C-terminally truncated constitutively active RopGEF7 (RopGEF7DC) activates RAC/ROP GTPases. Knockdown of RopGEF7 by RNA interference causes defects in embryo patterning and maintenance of the QC and leads to postembryonic loss of root stem cell population. Gene expression studies indicate that RopGEF7 is required for root meristem maintenance as it regulates the expression of PLETHORA1 (PLT1) and PLT2, which are key transcription factors that mediate the patterning of the root stem cell niche. Genetic analyses show that RopGEF7 interacts with PLT genes to regulate QC maintenance. Moreover, RopGEF7 is induced transcriptionally by auxin while its function is required for the expression of the auxin efflux protein PIN1 and maintenance of normal auxin maxima in embryos and seedling roots. These results suggest that RopGEF7 may integrate auxin-derived positional information in a feed-forward mechanism, regulating PLT transcription factors and thereby controlling the maintenance of root stem cell niches.