6 research outputs found

    Mucilage attachment to seeds provides evidence of a novel link between cellulose and pectin

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    In certain plant species, including Arabidopsis, seed coat epidermal cells accumulate a large quantity of polysaccharides that are released as mucilage upon imbibition. Once released, Arabidopsis seed coat mucilage appears as two distinct layers, the outer non-adherent composed of unsubstitutedrhamnogalacturonan I (RG-I), and the inner adherent one mainly made of RG-I and cellulose. CELLULOSE SYNTHASE5 and MUCILAGE-MODIFIED (MUM)5 have both been shown to be required for anchoring the mucilage pectin to the seed coat surface [1-5]. The identity and molecular role of MUM5 remained to be determined. A comparison of sequentially extracted seed mucilage components from cesa5 and mum5 mutants was carried out. Both mutants showed a redistribution of mucilage pectin from the inner adherent layer to the outer soluble one. cesa5 further showed a clear reduction in cellulose content, whereas mum5 had a wild-type cellulose content, but had reduced Xyl contents in the outer mucilage layer. Accordingly, MUM5 was identified as a putative xylosyltransferase. Biochemical and in vitro binding assay data demonstrated that xylan chains are attached to RG-I chains and mediate the adsorption of mucilage to cellulose microfibrils. The importance of having both a correctly synthesized cellulose scaffold and pectin structure will be discussed with regard to mucilage partitioning into non-adherent and adherent layers

    Xylans Provide the Structural Driving Force for Mucilage Adhesion to the Arabidopsis Seed Coat

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    International audienceArabidopsis (Arabidopsis thaliana) seed coat epidermal cells produce large amounts of mucilage that is released upon imbibition. This mucilage is structured into two domains: an outer diffuse layer that can be easily removed by agitation and an inner layer that remains attached to the outer seed coat. Both layers are composed primarily of pectic rhamnogalacturonan I (RG-I), the inner layer also containing rays of cellulose that extend from the top of each columella. Perturbation in cellulosic ray formation has systematically been associated with a redistribution of pectic mucilage from the inner to the outer layer, in agreement with cellulose-pectin interactions, the nature of which remained unknown. Here, by analyzing the outer layer composition of a series of mutant alleles, a tight proportionality of xylose, galacturonic acid, and rhamnose was evidenced, except for mucilage modified5-1 (mum5-1; a mutant showing a redistribution of mucilage pectin from the inner adherent layer to the outer soluble one), for which the rhamnose-xylose ratio was increased drastically. Biochemical and in vitro binding assay data demonstrated that xylan chains are attached to RG-I chains and mediate the adsorption of mucilage to cellulose microfibrils. mum5-1 mucilage exhibited very weak adsorption to cellulose. MUM5 was identified as a putative xylosyl transferase recently characterized as MUCI21. Together, these findings suggest that the binding affinity of xylose ramifications on RG-I to a cellulose scaffold is one of the factors involved in the formation of the adherent mucilage layer

    A systems biology approach uncovers a gene co-expression network associated with cell wall degradability in maize

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    Understanding the mechanisms triggering variation of cell wall degradability is a prerequisite to improving the energy value of lignocellulosic biomass for animal feed or biorefinery. Here, we implemented a multiscale systems approach to shed light on the genetic basis of cell wall degradability in maize. We demonstrated that allele replacement in two pairs of near-isogenic lines at a region encompassing a major quantitative trait locus (QTL) for cell wall degradability led to phenotypic variation of a similar magnitude and sign to that expected from a QTL analysis of cell wall degradability in the F271 Ă— F288 recombinant inbred line progeny. Using DNA sequences within the QTL interval of both F271 and F288 inbred lines and Illumina RNA sequencing datasets from internodes of the selected near-isogenic lines, we annotated the genes present in the QTL interval and provided evidence that allelic variation at the introgressed QTL region gives rise to coordinated changes in gene expression. The identification of a gene co-expression network associated with cell wall-related trait variation revealed that the favorable F288 alleles exploit biological processes related to oxidation-reduction, regulation of hydrogen peroxide metabolism, protein folding and hormone responses. Nested in modules of co-expressed genes, potential new cell-wall regulators were identified, including two transcription factors of the group VII ethylene response factor family, that could be exploited to fine-tune cell wall degradability. Overall, these findings provide new insights into the regulatory mechanisms by which a major locus influences cell wall degradability, paving the way for its map-based cloning in maize

    Signaling and sensing: the role of Class II TREHALOSE 6-PHOSPHATE SYNTHASE genes in suppression of eskimo1 dwarfism phenotype.

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    International audienceIn Arabidopsis, eskimo1 mutant is due to a mutation in XOAT1 gene (Xylan O-acetyl transferase 1). Its mutation leads to abnormal xylan acetylation resulting in collapsed xylem. This cell wall defect reduces water conductivity and generates constitutive plant stress leading to a dwarfism phenotype. This phenotype is supressed by a mutation in Class II TREHALOSE 6-PHOSPHATE SYNTHASE 7 (TPS 7) gene. The two closest homologous class II genes of TPS7, TPS5 and TPS6, were also investigated for esk1 dwarfism suppression. The results will be presented here

    Signaling and sensing: the role of Class II TREHALOSE 6-PHOSPHATE SYNTHASE genes in suppression of eskimo1 dwarfism phenotype.

    No full text
    International audienceIn Arabidopsis, eskimo1 mutant is due to a mutation in XOAT1 gene (Xylan O-acetyl transferase 1). Its mutation leads to abnormal xylan acetylation resulting in collapsed xylem. This cell wall defect reduces water conductivity and generates constitutive plant stress leading to a dwarfism phenotype. This phenotype is supressed by a mutation in Class II TREHALOSE 6-PHOSPHATE SYNTHASE 7 (TPS 7) gene. The two closest homologous class II genes of TPS7, TPS5 and TPS6, were also investigated for esk1 dwarfism suppression. The results will be presented here
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