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纤维素合成减少引发拟南芥的木质化和防御反应。

Reduced cellulose synthesis invokes lignification and defense responses in Arabidopsis thaliana.

作者信息

Caño-Delgado Ana, Penfield Steven, Smith Caroline, Catley Merryn, Bevan Michael

机构信息

Cell and Developmental Biology Department, John Innes Centre, Colney Lane, Norwich NR4 7UJ, UK.

出版信息

Plant J. 2003 May;34(3):351-62. doi: 10.1046/j.1365-313x.2003.01729.x.

Abstract

The cell wall determines the shape of plant cells and is also the primary interface for pathogen interactions. The structure of the cell wall can be modified in response to developmental and environmental cues, for example to strengthen the wall and to create barriers to pathogen ingress. The ectopic lignin 1-1 and 1-2 (eli1-1 and eli1-2) mutations lead to an aberrant deposition of lignin, a complex phenylpropanoid polymer. We show that the eli1 mutants occur in the cellulose synthase gene CESA3 in Arabidopsis thaliana and cause reduced cellulose synthesis, providing further evidence for the function of multiple CESA subunits in cellulose synthesis. We show that reduced levels of cellulose synthesis, caused by mutations in cellulose synthase genes and in genes affecting cell expansion, activate lignin synthesis and defense responses through jasmonate and ethylene and other signaling pathways. These observations suggest that mechanisms monitoring cell wall integrity can activate lignification and defense responses.

摘要

细胞壁决定了植物细胞的形状,也是病原体相互作用的主要界面。细胞壁的结构可根据发育和环境信号进行修饰,例如增强细胞壁并形成病原体侵入的屏障。异位木质素1-1和1-2(eli1-1和eli1-2)突变导致木质素异常沉积,木质素是一种复杂的苯丙烷聚合物。我们发现,拟南芥的eli1突变体发生在纤维素合酶基因CESA3中,并导致纤维素合成减少,这为多个CESA亚基在纤维素合成中的功能提供了进一步证据。我们表明,纤维素合酶基因和影响细胞扩张的基因发生突变导致纤维素合成水平降低,通过茉莉酸和乙烯以及其他信号通路激活木质素合成和防御反应。这些观察结果表明,监测细胞壁完整性的机制可以激活木质化和防御反应。

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