nitiation of ER Body Formation and Indole Glucosinolate Metabolism by the Plastidia Retrograde Signaling Metabolite, MEcPP
nitiation of ER Body Formation and Indole Glucosinolate Metabolism by the Plastidia Retrograde Signaling Metabolite, MEcPP作者机构:Institute for Integrative Genome Biology and Department of Botany and Plant Sciences University of California Riverside CA 92521 USA Department of Plant Biology University of California Davis CA 95616 USA Department of Plant Sciences University of California Davis CA 95616 USA Division of Biological Sciences University of California San Diego La Jolla CA 92093 USA Department of Cell and Metabolic Biology Leibniz-lnstitute of Plant Biochemistry Halle Germany Present address: College of Agronomy and Biotechnology Southwest University Chongqing P.R. China Present address: Rice Research Institute Sichuan Agricultural University Changdu Sichuan 611130 China
出 版 物:《Molecular Plant》 (分子植物(英文版))
年 卷 期:2017年第10卷第11期
页 面:1400-1416页
核心收录:
学科分类:0710[理学-生物学] 07[理学] 071009[理学-细胞生物学] 09[农学] 0901[农学-作物学] 090102[农学-作物遗传育种]
基 金:supported by National Science Foundation NIH to K.D
主 题:glucosinolates ER body retrograde signaling MEP pathway MEcPP stress
摘 要:Plants have evolved tightly regulated signaling networks to respond and adapt to environmental perturbations, but the nature of the signaling hub(s) involved have remained an enigma. We have previously established that methylerythritol cyclodiphosphate (MEcPP), a precursor of plastidial isoprenoids and a stress- specific retrograde signaling metabolite, enables cellular readjustments for high-order adaptive functions. Here, we specifically show that MEcPP promotes two Brassicaceae-specific traits, namely endoplasmic reticulum (ER) body formation and induction of indole glucosinolate (IGs) metabolism selectively, via tran- scriptional regulation of key regulators NAIl for ER body formation and MYB51/122 for IGs biosynthesis). The specificity of MEcPP is further confirmed by the lack of induction of wound-inducible ER body genes as well as IGs by other altered methylerythritol phosphate pathway enzymes. Genetic analyses revealed MEcPP-mediated COil-dependent induction of these traits. Moreover, MEcPP signaling integrates the biosynthesis and hydrolysis of IGs through induction of nitrile-specifier protein1 and reduction of the sup- pressor, ESM1, and production of simple nitriles as the bioactive end product. The findings position the plastidial metabolite, MEcPP, as the initiation hub, transducing signals to adjust the activity of hard- wired gene circuitry to expand phytochemical diversity and alter the associated subcellular structure required for functionality of the secondary metabolites, thereby tailoring plant stress responses.