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首页> 外文期刊>Plant Cell Reports >Transcriptional profiling in response to inhibition of cellulose synthesis by thaxtomin A and isoxaben in Arabidopsis thaliana suspension cells
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Transcriptional profiling in response to inhibition of cellulose synthesis by thaxtomin A and isoxaben in Arabidopsis thaliana suspension cells

机译:在拟南芥悬浮细胞中,响应于纤溶酶A和异恶草素抑制纤维素合成的转录谱

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摘要

The plant cell wall determines cell shape and is the main barrier against environmental challenges. Perturbations in the cellulose content of the wall lead to global modifications in cellular homeostasis, as seen in cellulose synthase mutants or after inhibiting cellulose synthesis. In particular, application of inhibitors of cellulose synthesis such as thaxtomin A (TA) and isoxaben (IXB) initiates a programmed cell death (PCD) in Arabidopsis thaliana suspension cells that is dependent on de novo gene transcription. To further understand how TA and IXB activate PCD, a whole genome microarray analysis was performed on mRNA isolated from Arabidopsis suspension cells exposed to TA and IXB. More than 75% of the genes upregulated by TA were also upregulated by IXB, including genes encoding cell wall-related and calcium-binding proteins, defence/stress-related transcription factors, signalling components and cell death-related proteins. Comparisons with published transcriptional analyses revealed that half of these genes were also induced by ozone, wounding, bacterial elicitor, Yariv reagent, chitin and H2O2. These data indicate that both IXB and TA activate a similar gene expression profile, which includes an important subset of genes generally induced in response to various biotic and abiotic stress. However, genes typically activated during the defence response mediated by classical salicylic acid, jasmonate or ethylene signalling pathways were not upregulated in response to TA and IXB. These results suggest that inhibition of cellulose synthesis induces PCD by the activation of common stress-related pathways that would somehow bypass the classical hormone-dependent defence pathways.
机译:植物细胞壁决定细胞的形状,并且是应对环境挑战的主要障碍。如在纤维素合酶突变体中或抑制纤维素合成后所见,壁中纤维素含量的扰动导致细胞稳态的整体改变。特别地,纤维素合成抑制剂的应用,例如thaxtomin A(TA)和异恶魔(IXB),在拟南芥悬浮细胞中启动了程序性细胞死亡(PCD),这取决于从头基因的转录。为了进一步了解TA和IXB如何激活PCD,对从暴露于TA和IXB的拟南芥悬浮细胞中分离的mRNA进行了全基因组微阵列分析。 IXB还上调了超过75%的TA上调的基因,包括编码细胞壁相关蛋白和钙结合蛋白,防御/应激相关转录因子,信号转导成分和细胞死亡相关蛋白的基因。与已发表的转录分析的比较表明,这些基因中的一半也被臭氧,创伤,细菌引发剂,Yariv试剂,几丁质和H 2 O 2 诱导。这些数据表明,IXB和TA均激活相似的基因表达谱,其中包括通常对各种生物和非生物胁迫的应答而诱导的重要基因子集。但是,通常在经典水杨酸,茉莉酸或乙烯信号传导途径介导的防御反应中被激活的基因并未响应TA和IXB而被上调。这些结果表明,纤维素合成的抑制通过激活常见的应激相关途径来诱导PCD,而这些途径将以某种方式绕过经典的激素依赖性防御途径。

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