Mitsuda Nobutaka, Seki Motoaki, Shinozaki Kazuo, Ohme-Takagi Masaru
Gene Function Research Center, National Institute of Advanced Industrial Science and Technology, Tsukuba, Ibaraki 305-8562, Japan.
Plant Cell. 2005 Nov;17(11):2993-3006. doi: 10.1105/tpc.105.036004. Epub 2005 Oct 7.
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.
在植物中,次生壁加厚在各种生物学过程中发挥着重要作用,尽管调节这些过程的因素仍有待确定。我们发现,在拟南芥中表达源自NAC次生壁加厚促进因子1(NST1)和NST2的嵌合阻遏物,会导致花药开裂缺陷,这是由于花药内皮细胞中次生壁加厚的丧失所致。NST1和NST2的双T-DNA标签系(而非单T-DNA标签系)的植物具有与表达单个嵌合阻遏物的转基因植物相同的花药不开裂表型,这表明NST1和NST2在调节花药壁次生壁加厚方面是冗余的。NST2启动子在花药组织中的活性特别强,而NST1启动子的活性在木质化次生壁发育的各种组织中都能检测到。NST1或NST2的异位表达诱导了地上各种组织中次生壁的异位加厚。次生壁异位加厚的表皮细胞具有与管状分子相似的结构特征。然而,在参与管状分子分化的基因中,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均未受到类似影响。我们的结果表明,NAC转录因子可能是各种组织中次生壁加厚的调节因子。