首页> 外文期刊>Planta: An International Journal of Plant Biology >Two NAC domain transcription factors, SND1 and NST1, function redundantly in regulation of secondary wall synthesis in fibers of Arabidopsis
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Two NAC domain transcription factors, SND1 and NST1, function redundantly in regulation of secondary wall synthesis in fibers of Arabidopsis

机译:两个NAC域转录因子SND1和NST1在拟南芥纤维的次级壁合成调节中起冗余作用

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Secondary walls are the major component of wood, and studies of the mechanisms regulating secondary wall synthesis is important for understanding the process of wood formation. We have previously shown that the NAC domain transcription factor SECONDARY WALL-ASSOCIATED NAC DOMAIN PROTEIN1 (SND1) is a key regulator of secondary wall synthesis in fibers of Arabidopsis thaliana stems and dominant repression of SND1 leads to a reduction in secondary wall thickening in fibers. However, T-DNA knockout of the SND1 gene did not cause an alteration in secondary wall thickness, suggesting that other SND1 homologs may compensate for the loss of SND1 expression. Here, we studied the effects of simultaneous inhibition of SND1 and its homolog, NAC SECONDARY WALL THICKENING PROMOTING FACTOR1 (NST1), on secondary wall synthesis in fibers. We show that simultaneous RNA interference (RNAi) inhibition of the expression of both SND1 and NST1 genes results in loss of secondary wall formation in fibers of stems. The fiber cells in the stems of SND1/NST1-RNAi plants lack all three major secondary wall components, including cellulose, xylan, and lignin, which is accompanied by a severe reduction in the expression of genes involved in their biosynthesis. In addition, inhibition of SND1 and NST1 leads to down-regulation of several fiber-associated transcription factor genes. Double T-DNA knockout mutations of SND1 and NST1 genes cause the same effects, as does simultaneous RNAi inhibition of SND1 and NST1. Our results provide first line evidence demonstrating that SND1 and NST1 function redundantly in the regulation of secondary wall synthesis in fibers.
机译:次生壁是木材的主要组成部分,对调节次生壁合成机制的研究对于理解木材形成过程非常重要。先前我们已经表明,NAC结构域转录因子第二壁相关NAC域蛋白1(SND1)是拟南芥茎纤维中次生壁合成的关键调节剂,SND1的显性抑制导致纤维中次生壁增厚的减少。但是,敲除SND1基因的T-DNA并未引起次级壁厚度的改变,这表明其他SND1同源物可能弥补了SND1表达的损失。在这里,我们研究了同时抑制SND1及其同系物NAC次生壁增厚促进因子1(NST1)对纤维中次生壁合成的影响。我们表明同时RNA干扰(RNAi)SND1和NST1基因表达的抑制作用导致茎纤维中次生壁形成的损失。 SND1 / NST1-RNAi植物茎中的纤维细胞缺乏所有三个主要的次生壁成分,包括纤维素,木聚糖和木质素,伴随着其生物合成相关基因的表达大大降低。此外,对SND1和NST1的抑制会导致一些与纤维相关的转录因子基因的下调。 SND1和NST1基因的双重T-DNA敲除突变引起相同的效果,同时RNAi抑制SND1和NST1也是如此。我们的结果提供了一线证据,证明SND1和NST1在调节纤维中次生壁的合成中起着多余的作用。

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