16 research outputs found

    Biotechnology in trees: towards improved paper pulping by lignin engineering

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    Lignin is a heterogenous phenolic polymer that plays crucial roles in the development and physiology of vascular plants. However, it needs to be removed from cellulose by toxic and energy-requiring processes for the production of high-quality paper. Therefore, a major biotechnological challenge is to obtain transgenic trees with modified lignin to improve the quality of wood for paper making. Here, we review the results obtained by alterating the expression of genes of the monolignol biosynthesis pathway in trees and the effect of these modifications on the lignin polymer and on pulping. The data reported show that lignin engineering is a promising strategy to improve wood quality for the pulp and paper industry.info:eu-repo/semantics/publishe

    A systems biology view of responses to lignin biosynthesis perturbations in <em>Arabidopsis</em>

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    Lignin engineering is an attractive strategy to improve lignocellulosic biomass quality for processing to biofuels and other bio-based products. However, lignin engineering also results in profound metabolic consequences in the plant. We used a systems biology approach to study the plant's response to lignin perturbations. To this end, inflorescence stems of 20 Arabidopsis thaliana mutants, each mutated in a single gene of the lignin biosynthetic pathway (phenylalanine ammonia-lyase1 [PAL1], PAL2, cinnamate 4-hydroxylase [C4H], 4-coumarate:CoA ligase1 [4CL1], 4CL2, caffeoyl-CoA O-methyltransferase1 [CCoAOMT1], cinnamoyl-CoA reductase1 [CCR1], ferulate 5-hydroxylase [F5H1], caffeic acid O-methyltransferase [COMT], and cinnamyl alcohol dehydrogenase6 [CAD6], two mutant alleles each), were analyzed by transcriptomics and metabolomics. A total of 566 compounds were detected, of which 187 could be tentatively identified based on mass spectrometry fragmentation and many were new for Arabidopsis. Up to 675 genes were differentially expressed in mutants that did not have any obvious visible phenotypes. Comparing the responses of all mutants indicated that c4h, 4cl1, ccoaomt1, and ccr1, mutants that produced less lignin, upregulated the shikimate, methyl-donor, and phenylpropanoid pathways (i.e., the pathways supplying the monolignols). By contrast, f5h1 and comt, mutants that provoked lignin compositional shifts, downregulated the very same pathways. Reductions in the flux to lignin were associated with the accumulation of various classes of 4-O- and 9-O-hexosylated phenylpropanoids. By combining metabolomic and transcriptomic data in a correlation network, system-wide consequences of the perturbations were revealed and genes with a putative role in phenolic metabolism were identified. Together, our data provide insight into lignin biosynthesis and the metabolic network it is embedded in and provide a systems view of the plant's response to pathway perturbations

    Applications of molecular genetics for biosynthesis of novel lignins

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    For the production of high-quality paper, lignin needs to be removed from cellulose. This process is energy requiring, expensive and toxic. Molecular biology offers tools to generate trees with a modified lignin composition to facilitate the extractability of lignin. We have cloned several genes encoding enzymes in the methylation of the lignin monomers [bi-specific caffeic acid/5-hydroxyferulic acid O-methyltransferase (COMT) and caffeoyl-CoA O-methyltransferase], and encoding enzymes specific for the lignin biosynthesis pathway [cinnamoyl-CoA reductase and cinnamyl alcohol dehydrogenase (CAD)]. The antisense strategy is used to study the effect of a down-regulation of these enzymes on the lignin content and the lignin composition of poplar wood. Our results demonstrate that the monomeric composition of lignin was dramatically affected by down-regulation of COMT. Transgenic poplars with a reduced CAD activity have better pulping properties, due to a higher extractability of the lignin. © 1998 Elsevier Science Limited. All rights reserved.info:eu-repo/semantics/publishe
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