The NAC transcription factors NST1 and NST2 of Arabidopsis regulate secondary wall thickenings and are required for anther dehiscence
The NAC transcription factors NST1 and NST2 of Arabidopsis regulate secondary wall thickenings and are required for anther dehiscence
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DOI：
10.1105/tpc.105.036004
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发表时间：
2005-11-01
期刊：
影响因子：
11.6
通讯作者：
Ohme-Takagi, M
中科院分区：
文献类型：
--
作者：
Mitsuda, N;Seki, M;Ohme-Takagi, M
在植物中，次生壁增厚在各种生物学过程中起着重要作用，尽管调节这些过程的因素仍有待于表征。我们表明，嵌合阻遏物来自NAC次生壁增厚促进因子1（NST 1）和NST 2在拟南芥中的表达导致花药开裂缺陷，由于损失的次生壁增厚在花药药室内壁。植物与双，但不是单一的，T-DNA标记线NST 1和NST 2具有相同的花药不裂表型的转基因植物表达的个人嵌合阻遏物，表明NST 1和NST 2是多余的，在调节次生壁加厚花药壁。NST 2启动子的活性在花药组织中特别强，而NST 1启动子的活性在其中发育有木质部次生壁的各种组织中检测到。NST 1或NST 2的异位表达诱导各种地上组织中次生壁的异位增厚。具有次生壁异位增厚的表皮细胞具有与管分子相似的结构特征。然而，在参与导管分子分化的基因中，只有那些与次生壁合成相关的基因明显上调。参与程序性细胞死亡的基因都没有受到类似的影响。我们的研究结果表明，NAC转录因子作为可能的监管机构在各种组织中的次生壁增厚。
In plants, secondary wall thickenings play important roles in various biological processes, although the factors regulating these processes remain to be characterized. We show that expression of chimeric repressors derived from NAC SECONDARY WALL THICKENING PROMOTING FACTOR1 (NST1) and NST2 in Arabidopsis thaliana resulted in an anther dehiscence defect due to loss of secondary wall thickening in anther endothecium. Plants with double, but not single, T-DNA-tagged lines for NST1 and NST2 had the same anther-indehiscent phenotype as transgenic plants that expressed the individual chimeric repressors, indicating that NST1 and NST2 are redundant in regulating secondary wall thickening in anther walls. The activity of the NST2 promoter was particularly strong in anther tissue, while that of the NST1 promoter was detected in various tissues in which lignified secondary walls develop. Ectopic expression of NST1 or NST2 induced ectopic thickening of secondary walls in various aboveground tissues. Epidermal cells with ectopic thickening of secondary walls had structural features similar to those of tracheary elements. However, among genes involved in the differentiation of tracheary elements, only those related to secondary wall synthesis were clearly upregulated. None of the genes involved in programmed cell death were similarly affected. Our results suggest NAC transcription factors as possible regulators of secondary wall thickening in various tissues.