| Title: | Negative regulation of plastidial isoprenoid pathway by herbivore-induced beta-cyclocitral in Arabidopsis thaliana |
| Author(s): | Mitra S; Estrada-Tejedor R; Volke DC; Phillips MA; Gershenzon J; Wright LP; |
| Address: | "Department of Biochemistry, Max Planck Institute for Chemical Ecology, 07745 Jena, Germany; smitra@unipune.ac.in lwright@tutanota.com. Department of Botany, Savitribai Phule Pune University, Pune-411007, India. Pharmaceutical Chemistry Group, IQS School of Engineering, Universitat Ramon Llull, 08017 Barcelona, Spain. The Novo Nordisk Foundation Center for Biosustainability, Technical University of Denmark, 2800 Kongens Lyngby, Denmark. Department of Biology, University of Toronto Mississauga, Mississauga, ON L5L 1C6, Canada. Department of Biochemistry, Max Planck Institute for Chemical Ecology, 07745 Jena, Germany" |
| ISSN/ISBN: | 1091-6490 (Electronic) 0027-8424 (Print) 0027-8424 (Linking) |
| Abstract: | "Insect damage to plants is known to up-regulate defense and down-regulate growth processes. While there are frequent reports about up-regulation of defense signaling and production of defense metabolites in response to herbivory, much less is understood about the mechanisms by which growth and carbon assimilation are down-regulated. Here we demonstrate that insect herbivory down-regulates the 2-C-methyl-D-erythritol-4-phosphate (MEP) pathway in Arabidopsis (Arabidopsis thaliana), a pathway making primarily metabolites for use in photosynthesis. Simulated feeding by the generalist herbivore Spodoptera littoralis suppressed flux through the MEP pathway and decreased steady-state levels of the intermediate 1-deoxy-D-xylulose 5-phosphate (DXP). Simulated herbivory also increased reactive oxygen species content which caused the conversion of beta-carotene to beta-cyclocitral (betaCC). This volatile oxidation product affected the MEP pathway by directly inhibiting DXP synthase (DXS), the rate-controlling enzyme of the MEP pathway in Arabidopsis and inducing plant resistance against S. littoralis betaCC inhibited both DXS transcript accumulation and DXS activity. Molecular models suggested that betaCC binds to DXS at the binding site for the thymine pyrophosphate cofactor and blocks catalysis, which was confirmed by direct assays of betaCC with the purified DXS protein in vitro. Another intermediate of the MEP pathway, 2-C-methyl-D-erythritol-2, 4-cyclodiphosphate, which is known to stimulate salicylate defense signaling, showed greater accumulation and enhanced export out of the plastid in response to simulated herbivory. Together, our work implicates betaCC as a signal of herbivore damage in Arabidopsis that increases defense and decreases flux through the MEP pathway, a pathway involved in growth and carbon assimilation" |
| Keywords: | Aldehydes/*pharmacology Arabidopsis/*metabolism Diterpenes/*pharmacology Herbivory Plastids/*pathology Terpenes/*metabolism apocarotenoids isoprenoid mechanical damage methylerythritol-4-phosphate pathway simulated herbivory; |
| Notes: | "MedlineMitra, Sirsha Estrada-Tejedor, Roger Volke, Daniel C Phillips, Michael A Gershenzon, Jonathan Wright, Louwrance P eng Research Support, Non-U.S. Gov't 2021/03/07 Proc Natl Acad Sci U S A. 2021 Mar 9; 118(10):e2008747118. doi: 10.1073/pnas.2008747118" |
