Signaling of reactive oxylipins in plants
Final Report Abstract
Biotic and abiotic stresses result in an accumulation of oxylipins in plants. The oxylipin 12- oxophytodienoic acid belongs to the group of reactive electrophile species (RES). Several stresses and application of RES-oxylipins from plant or animal origin activate defense and detoxification mechanisms. However, little is known about the signaling pathway which mediates these responses. The main aim of this project was to identify components of this new signaling pathway. This was addressed by a forward genetic approach with mutants of Arabidopsis thaliana which show an altered response to RES-oxylipins. In addition, characterization of stress-related phenotypes of the mutant was persued to elucidate the function of RES-oxylipins in stress responses. The mutation causative for the lower responsiveness of the nr1 mutant to RES-oxylipins was identified to be in a gene encoding a putative transcription factor. It was shown that the phenotype is not based on a defect in oxylipin biosynthesis and that the lower responsiveness is specific for RES- oxylipins. The transcriptome analysis indicates that the transcription factor contributes to the cross talk with salicylic acid signaling and the signaling pathway dependent on TGA transcription factors. The resistance of this mutant to bacterial and fungal pathogens was slightly altered. A defect in the transcription factor enhanced the sensitivity to oxidative stress. Lines overexpressing the transcription factor were generated and can be used in the future to further explore the function of this protein. The knowledge gained on RES-oxylipin signaling might contribute to understanding and manipulating stress resistance in plants in the future.
Publications
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(2018) Mutanten im RES-Oxylipin Signalweg von Arabidopsis thaliana, Dissertationsschrift, Julius-Maximilians-Universität Würzburg
Manuel Lange
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(2018) TGA2 signaling in response to reactive electrophile species is not dependent on cysteine modification of TGA2. PLoS One 13, e0195398
S. Findling, HU. Stotz, M. Zoeller, M. Krischke, M. Zander, C. Gatz, S. Berger, MJ. Mueller
