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Rautengarten, C.

Publications and source records attributed to Rautengarten, C..

3 recordsLinked to original sources

Galactan mobilization during carbon starvation compromises cell wall-mediated fungal resistance in Arabidopsis

Polysaccharides are the main components present in plant cell walls. They form a network that is dynamically modified during growth and upon both abiotic and biotic stress. We investigated how the cell wall of Arabidopsis rosettes is remodeled during periods of dark-induced starvation in the wild type and in plastidic phosphoglucomutase (pgm) mutants, which suffer from periodic starvation due to starch deficiency. Time-course analysis demonstrated that up to one fifth of the galactose present in leaf cell walls is reversibly released upon starvation, while other cell wall monosaccharides were less affected. An investigation of BETA-GALACTOSIDASE (BGAL) expression and the analysis of bgal mutants indicated that BGAL1 and BGAL4 contribute to the release of cell wall galactose upon starvation. Increased transcript abundance of UDP-GLUCOSE 4-EPIMERASE (UGE) 1 and 3 under starvation proposed an increased flux through the galactose salvage pathway, however an analysis of the UDP- galactose pool in mutant plants indicated redundancy with other UGEs. Simultaneously to galactan degradation, GALACTAN SYNTHASE1 (GALS1) expression was reduced, attenuating the synthesis of new galactan chains. We show that overexpression of GALS1 prevents depletion of the recyclable cell wall galactose pool and is sufficient to rescue impaired penetration resistance to the hemibiotrophic fungal pathogen Colletotrichum higginsianum upon dark-induced and periodic starvation. Our data suggest that pectic galactan in the plant cell wall serves as a sugar resource during starvation conditions. However, galactose release from the wall leads to impaired penetration resistance against a fungal pathogen, causing a tradeoff between sugar supply for plant metabolism and preformed defense. Significance statementPolysaccharides present in plant cell walls must be dynamically modified in response to external stimuli, but it is not well understood how cell wall remodeling is adjusted in response to metabolic cues and how this affects defense against pathogens. Here, we report that galactose is reversibly released from cell walls upon carbon starvation, which critically affects penetration resistance to a fungal pathogen.

plant biology↗

The Building Blocks of Early Land Plants: Glycosyltransferases and Cell Wall Architecture in the model liverwort Marchantia polymorpha

The liverwort Marchantia polymorpha has emerged as an important plant model for developmental studies and may become central to elucidate the complex process of cell wall polysaccharide biosynthesis. This study comprehensively analyses the composition and structure of cell wall glycans across eight different M. polymorpha tissue types. We show that while the cell walls largely mirror known land plant cell wall composition, they also exhibit some unique characteristics. For example, -(1,5)-arabinan was prominently present in the sporophyte tissue, which may indicate a specialised role in this life stage. Furthermore, M. polymorpha cell walls displayed a remarkably low overall pectin content, yet the abundance of pectic arabinan in sporophytes hint at its putative role in the evolution and complexity of spermatophyte cell walls. Through comparative analyses of glycosyltransferase (GT) families across plant species, we found that M. polymorpha has a diversified GT repertoire compared for example, to the model plant Arabidopsis thaliana, indicating uniqueness in its cell wall biosynthesis pathways. To support research underpinning cell wall biosynthesis, we developed a Gateway compatible compendium of 93 M. polymorpha GTs, providing a valuable resource for genetic and functional studies. Our study thus works as a foundation to drive new insights into cell wall evolution, structure and function across the plant kingdom.

plant biology↗

Disrupted copper availability in sporadic ALS: Implications for CuII(atsm) as a treatment option

ObjectiveThe copper compound CuII(atsm) is in phase 2/3 testing for treatment of the neurodegenerative disease amyotrophic lateral sclerosis (ALS). CuII(atsm) consistently and reproducibly ameliorates neurodegeneration in mutant SOD1 mouse models of ALS where its neuroprotective activity has been ascribed in part to improving availability of copper to essential cuproenzymes. However, SOD1 mutations cause only ~2% of ALS cases with most cases being of unknown aetiology. Therapeutic pertinence of CuII(atsm) to sporadic ALS is therefore unclear. MethodsWe assayed post-mortem spinal cord tissue from sporadic cases of ALS for the anatomical and biochemical distribution of copper, the expression of genes involved in copper handling, and the activities of cuproenzymes. ResultsThe natural distribution of copper is disrupted in sporadic ALS. The ALS-affected tissue has a molecular signature consistent with an unsatiated requirement for copper and cuproenzyme activity is affected. Copper levels are decreased in the ventral grey matter, the primary anatomical site of neuronal loss in ALS. InterpretationMice expressing mutant SOD1 recapitulate salient features of ALS. The unsatiated requirement for copper that is evident in these mice is a biochemical target for CuII(atsm). Evidences provided here for disrupted copper bioavailability in human cases of sporadic ALS indicate that a therapeutic mechanism for CuII(atsm) involving copper bioavailability is pertinent to sporadic cases of ALS, and not just those involving mutant SOD1.

neuroscience↗