Biology subjects

Munzert-Eberlein, K. S.

Publications and source records attributed to Munzert-Eberlein, K. S..

3 recordsLinked to original sources

bioRxiv2026

Defining the Xanthomonas euvesicatoria type II-secreted effector arsenal: core nutritional functions and effector diversity

O_LIThe type II secretion (T2S) system is conserved across the Xanthomonas lineage, yet its contributions to pathogenicity and secreted protein repertoires are poorly defined. We demonstrate that T2S systems in Xanthomonas pathovars with divergent hosts and lifestyles are required for disease. C_LIO_LIIn planta quantification of cell wall compositional changes during infection by Xanthomonas euvesicatoria (Xe) revealed that T2S-dependent depletion of galacturonic acid occurs during host colonization, providing experimental evidence for T2 effector (T2E)-mediated cell wall remodeling. C_LIO_LIUsing an in planta label-free proteomics approach, we identified two known and 20 new Xe T2Es from tomato apoplast, many with annotated functions in polysaccharide and protein cleavage. Growth assays on plant cell wall extracts and purified substrates revealed T2S-mediated metabolization of plant cell wall polysaccharides and proteins not only by Xe, but also by Xanthomonas axonopodis pv. glycines (Xag) and Xanthomonas campestris pv. campestris (Xcc). Interestingly, comparative sequence analysis revealed that the T2E repertoires have diversified among these pathogens, with differences in protease repertoire being the most pronounced. C_LIO_LIOur methodology establishes a framework for T2E discovery, enabling future functional dissection of this understudied effector class and its crosstalk with other bacterial virulence factors. C_LI

plant biology↗

bioRxiv2025

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↗

bioRxiv2025

Endogenous RALF peptide function is required for powdery mildew host colonization

The receptor kinase FERONIA (FER) is a susceptibility factor for biotrophic powdery mildew fungal pathogens in Arabidopsis thaliana, but the underlying molecular mechanisms remain largely unknown. FER is required for the perception of endogenous RAPID ALKALINIZATION FACTOR (RALF) peptides to control various aspects of plant growth, development and immunity. RALFs are perceived by FER-LORELEI-LIKE GPI-ANCHORED PROTEIN (LLG) heterocomplexes to induce cellular responses and bind to LEUCINE-RICH REPEAT EXTENSIN (LRX) proteins as structural components of the cell wall. Combining genetics, cell biology and biochemistry, we found that FERs endogenous RALF ligands are necessary for full colonization success of the powdery mildew species Erysiphe cruciferarum. We reveal that LLGs and LRXs are also powdery mildew susceptibility factors. We show that cell wall remodeling and apoplastic pH homeostasis, hallmark features of RALF function, support powdery mildew reproductive success. Moreover, we provide data that RALF-dependent powdery mildew pathogenesis is partially independent of FER. Powdery mildew fungi likely do not produce RALF peptide mimics, suggesting their reliance on endogenous RALFs for successful host colonization. We propose that powdery mildew fungi require RALF-mediated modulation of apoplastic pH and pectin re-modelling for successful host colonization, highlighting a new susceptibility mechanism by obligate biotrophic fungi.

plant biology↗