α‐1,3‐Glucan Is Required for Cell Wall Integrity and Full Virulence of Colletotrichum graminicola, but Not for Evasion of PAMP‐Triggered Immunity
7 affiliations
- 1Faculty of Natural Sciences III, Institute for Agricultural and Nutritional Sciences, Chair for Phytopathology and Plant Protection Martin‐Luther‐University Halle‐Wittenberg Halle (Saale) Germany
- 2Leibniz Institute of Plant Genetics and Crop Plant Research (IPK) OT Gatersleben Seeland Germany
- 3Faculty of Natural Sciences I, Institute for Biochemistry and Biotechnology Martin‐Luther‐University Halle‐Wittenberg Halle (Saale) Germany
- 4Fraunhofer Institute for Microstructure of Materials and Systems IMWS Halle (Saale) Germany
- 5Department Biology, Molecular Plant Physiology Marburg University Marburg Germany
- 6Center for Synthetic Microbiology (SYNMIKRO), Marburg University Marburg Germany
- 7Faculty of Life Sciences, Department of Biotechnology Ritsumeikan University Kusatsu Japan
Abstract
Although α‐1,3‐glucan represents a major polymer in cell walls of filamentous plant pathogenic fungi, its role in vegetative and pathogenic development is poorly understood. The maize anthracnose fungus Colletotrichum graminicola differentiates elaborate appressoria on the leaf surface and exhibits a hemibiotrophic lifestyle after host invasion. Promoter‐eGFP‐fusion analyses of all three α‐1,3‐glucan synthase (AGS) genes, designated as AGS1, AGS2, and AGS3, suggest that AGS3 is expressed in vegetative and pathogenic hyphae, whereas expression of AGS1 and AGS2 was not, or barely, detectable. Targeted gene deletions yielded single and double deletion mutants, as well as triple mutants, which lacked the entire repertoire of α‐1,3‐glucan synthase genes. Conidia of mutants lacking AGS3 developed multiple germ tubes, and vegetative hyphae had cell walls containing strongly reduced amounts of alkali‐soluble glucose, showed hyperbranching, reduced growth rates on all substrata tested, and hypersensitivity to the cell wall‐perturbing agents Caspofungin and Nikkomycin Z. Moreover, mutants lacking AGS3 exhibited strong virulence defects and, intriguingly, biotrophic hyphae of these mutants that differentiated in planta were severely misshapen. Increased cell wall pore diameters, increased mobility of uncharged dextran‐FITC conjugates through cell walls of AGS3‐deficient mutants and lack of PAMP‐triggered immune responses in maize leaves inoculated with these mutants suggest that α‐1,3‐glucan does not play a role in masking of fungal cell walls and immune evasion, but rather controls mobility of fungal cell wall‐modifying enzymes and cell wall integrity.
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BibTeX
@article{gase2026α13glucan,
title = {{α‐1,3‐Glucan Is Required for Cell Wall Integrity and Full Virulence of Colletotrichum graminicola, but Not for Evasion of PAMP‐Triggered Immunity}},
author = {Iris Gase and Lala Aliyeva‐Schnorr and Michael Melzer and Maria Ott and Julia Haufe and Matthias Menzel and Timo Engelsdorf and Christiane Rohrbach and Alan de Oliveira Silva and Lars M. Voll and Alexander S. Mickel and Maximilian Groß and Mamoru Wakayama and Holger B. Deising},
journal = {Molecular Microbiology},
year = {2026},
month = sep,
doi = {10.1111/mmi.70114},
url = {https://doi.org/10.1111/mmi.70114},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - α‐1,3‐Glucan Is Required for Cell Wall Integrity and Full Virulence of Colletotrichum graminicola, but Not for Evasion of PAMP‐Triggered Immunity
AU - Iris Gase
AU - Lala Aliyeva‐Schnorr
AU - Michael Melzer
AU - Maria Ott
AU - Julia Haufe
AU - Matthias Menzel
AU - Timo Engelsdorf
AU - Christiane Rohrbach
AU - Alan de Oliveira Silva
AU - Lars M. Voll
AU - Alexander S. Mickel
AU - Maximilian Groß
AU - Mamoru Wakayama
AU - Holger B. Deising
PY - 2026
DA - 2026/09/10
JO - Molecular Microbiology
DO - 10.1111/mmi.70114
UR - https://doi.org/10.1111/mmi.70114
AB - Although α‐1,3‐glucan represents a major polymer in cell walls of filamentous plant pathogenic fungi, its role in vegetative and pathogenic development is poorly understood. The maize anthracnose fungus Colletotrichum graminicola differentiates elaborate appressoria on the leaf surface and exhibits a hemibiotrophic lifestyle after host invasion. Promoter‐eGFP‐fusion analyses of all three α‐1,3‐glucan synthase (AGS) genes, designated as AGS1, AGS2, and AGS3, suggest that AGS3 is expressed in vegetative and pathogenic hyphae, whereas expression of AGS1 and AGS2 was not, or barely, detectable. Targeted gene deletions yielded single and double deletion mutants, as well as triple mutants, which lacked the entire repertoire of α‐1,3‐glucan synthase genes. Conidia of mutants lacking AGS3 developed multiple germ tubes, and vegetative hyphae had cell walls containing strongly reduced amounts of alkali‐soluble glucose, showed hyperbranching, reduced growth rates on all substrata tested, and hypersensitivity to the cell wall‐perturbing agents Caspofungin and Nikkomycin Z. Moreover, mutants lacking AGS3 exhibited strong virulence defects and, intriguingly, biotrophic hyphae of these mutants that differentiated in planta were severely misshapen. Increased cell wall pore diameters, increased mobility of uncharged dextran‐FITC conjugates through cell walls of AGS3‐deficient mutants and lack of PAMP‐triggered immune responses in maize leaves inoculated with these mutants suggest that α‐1,3‐glucan does not play a role in masking of fungal cell walls and immune evasion, but rather controls mobility of fungal cell wall‐modifying enzymes and cell wall integrity.
SN - 0950-382X
SN - 1365-2958
ER -