Journal
NATURE
Volume 509, Issue 7500, Pages 376-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature13084
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Funding
- Division of Chemical Sciences, Geosciences, and Biosciences, Office of Basic Energy Sciences of the US Department of Energy (DOE) [DE-FG02-07ER15905]
- Life Sciences Research Foundation
- US DOE Great Lakes Bioenergy Research Center (DOE BER Office of Science) [DE-FC02-07ER64944]
- Center for Direct Catalytic Conversion of Biomass to Biofuels (C3Bio), an Energy Frontier Research Center - US DOE, Office of Science, Office of Basic Energy Sciences [DE-SC0000997]
- US DOE [DE-FG02-06ER64301]
- Purdue University Office of Agricultural Research Programs
- Bioinformatics Core at Purdue University
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Lignin is a phenylpropanoid-derived heteropolymer important for the strength and rigidity of the plant secondary cell wall(1,2). 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(3). 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.
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