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破坏中介体拯救木质素缺陷拟南芥突变体的生长迟缓。

Disruption of Mediator rescues the stunted growth of a lignin-deficient Arabidopsis mutant.

机构信息

1] Department of Biochemistry, Purdue University, West Lafayette, Indiana 47907, USA [2] Dow AgroSciences LLC, 9330 Zionsville Road, Indianapolis, Indiana 46268, USA (N.D.B.); Department of Agronomy, University of Wisconsin-Madison, 1575 Linden Drive, Madison, Wisconsin 53706, USA (J.M.).

Department of Biochemistry, Purdue University, West Lafayette, Indiana 47907, USA.

出版信息

Nature. 2014 May 15;509(7500):376-80. doi: 10.1038/nature13084. Epub 2014 Mar 16.

DOI:10.1038/nature13084
PMID:24670657
Abstract

Lignin is a phenylpropanoid-derived heteropolymer important for the strength and rigidity of the plant secondary cell wall. Genetic disruption of lignin biosynthesis has been proposed as a means to improve forage and bioenergy crops, but frequently results in stunted growth and developmental abnormalities, the mechanisms of which are poorly understood. Here we show that the phenotype of a lignin-deficient Arabidopsis mutant is dependent on the transcriptional co-regulatory complex, Mediator. Disruption of the Mediator complex subunits MED5a (also known as REF4) and MED5b (also known as RFR1) rescues the stunted growth, lignin deficiency and widespread changes in gene expression seen in the phenylpropanoid pathway mutant ref8, without restoring the synthesis of guaiacyl and syringyl lignin subunits. Cell walls of rescued med5a/5b ref8 plants instead contain a novel lignin consisting almost exclusively of p-hydroxyphenyl lignin subunits, and moreover exhibit substantially facilitated polysaccharide saccharification. These results demonstrate that guaiacyl and syringyl lignin subunits are largely dispensable for normal growth and development, implicate Mediator in an active transcriptional process responsible for dwarfing and inhibition of lignin biosynthesis, and suggest that the transcription machinery and signalling pathways responding to cell wall defects may be important targets to include in efforts to reduce biomass recalcitrance.

摘要

木质素是一种苯丙烷衍生的杂聚物,对于植物次生细胞壁的强度和刚性很重要。遗传破坏木质素生物合成已被提议作为提高饲料和生物能源作物的一种手段,但经常导致生长迟缓和发育异常,其机制尚不清楚。在这里,我们表明木质素缺陷型拟南芥突变体的表型依赖于转录共调节复合物 Mediator。破坏 Mediator 复合物亚基 MED5a(也称为 REF4)和 MED5b(也称为 RFR1)可挽救矮化生长、木质素缺乏以及苯丙烷途径突变体 ref8 中所见的广泛基因表达变化,而不会恢复愈创木基和丁香基木质素亚基的合成。挽救的 med5a/5b ref8 植物的细胞壁反而含有一种新型木质素,几乎仅由 p-羟基苯基木质素亚基组成,而且表现出明显的多糖糖化促进作用。这些结果表明,愈创木基和丁香基木质素亚基在正常生长和发育中在很大程度上是可有可无的,暗示 Mediator 参与了一个负责矮化和抑制木质素生物合成的活跃转录过程,并表明响应细胞壁缺陷的转录机制和信号通路可能是减少生物质抗降解性努力中的重要目标。

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