Journal article
Authors list: Doehlemann, Gunther; Wahl, Ramon; Horst, Robin J.; Voll, Lars M.; Usadel, Bjoern; Poree, Fabien; Stitt, Mark; Pons-Kuehnemann, Joern; Sonnewald, Uwe; Kahmann, Regine; Kaemper, Joerg
Publication year: 2008
Pages: 181-195
Journal: The Plant Journal
Volume number: 56
Issue number: 2
ISSN: 0960-7412
DOI Link: https://doi.org/10.1111/j.1365-313X.2008.03590.x
Publisher: Wiley
Abstract:
The fungal pathogen Ustilago maydis establishes a biotrophic relationship with its host plant maize (Zea mays). Hallmarks of the disease are large plant tumours in which fungal proliferation occurs. Previous studies suggested that classical defence pathways are not activated. Confocal microscopy, global expression profiling and metabolic profiling now shows that U. maydis is recognized early and triggers defence responses. Many of these early response genes are downregulated at later time points, whereas several genes associated with suppression of cell death are induced. The interplay between fungus and host involves changes in hormone signalling, induction of antioxidant and secondary metabolism, as well as the prevention of source leaf establishment. Our data provide novel insights into the complexity of a biotrophic interaction.
Citation Styles
Harvard Citation style: Doehlemann, G., Wahl, R., Horst, R., Voll, L., Usadel, B., Poree, F., et al. (2008) Reprogramming a maize plant: transcriptional and metabolic changes induced by the fungal biotroph Ustilago maydis, The Plant Journal, 56(2), pp. 181-195. https://doi.org/10.1111/j.1365-313X.2008.03590.x
APA Citation style: Doehlemann, G., Wahl, R., Horst, R., Voll, L., Usadel, B., Poree, F., Stitt, M., Pons-Kuehnemann, J., Sonnewald, U., Kahmann, R., & Kaemper, J. (2008). Reprogramming a maize plant: transcriptional and metabolic changes induced by the fungal biotroph Ustilago maydis. The Plant Journal. 56(2), 181-195. https://doi.org/10.1111/j.1365-313X.2008.03590.x
Keywords
CORN SMUT FUNGUS; defence signalling; GLUTATHIONE-S-TRANSFERASES; LIGNIN BIOSYNTHESIS; PATHOGENIC DEVELOPMENT; PROGRAMMED CELL-DEATH; RESPONSE PATHWAYS; STRESS RESPONSES