Sulfur deficiency-induced repressor proteins optimize glucosinolate biosynthesis in plants.

Autor: Aarabi F; Max Planck Institute of Molecular Plant Physiology, Am Mühlenberg 1, 14476 Potsdam-Golm, Germany., Kusajima M; Faculty of Bioscience, Fukui Prefectural University, 4-1-1 Kenjojima, Matsuoka, Eiheiji-town, Fukui 910-1195, Japan., Tohge T; Max Planck Institute of Molecular Plant Physiology, Am Mühlenberg 1, 14476 Potsdam-Golm, Germany.; RIKEN Plant Science Center, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan., Konishi T; Department of Bioresource Sciences, Akita Prefectural University, Shimoshinjyo-Nakano, Akita 010-0195, Japan., Gigolashvili T; Botanical Institute, University of Cologne, Biocenter, Zuelpicher Str. 47 B, 50674 Cologne, Germany., Takamune M; RIKEN Plant Science Center, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan., Sasazaki Y; RIKEN Plant Science Center, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan., Watanabe M; Max Planck Institute of Molecular Plant Physiology, Am Mühlenberg 1, 14476 Potsdam-Golm, Germany., Nakashita H; Faculty of Bioscience, Fukui Prefectural University, 4-1-1 Kenjojima, Matsuoka, Eiheiji-town, Fukui 910-1195, Japan., Fernie AR; Max Planck Institute of Molecular Plant Physiology, Am Mühlenberg 1, 14476 Potsdam-Golm, Germany., Saito K; RIKEN Plant Science Center, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan.; Graduate School of Pharmaceutical Sciences, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8675, Japan., Takahashi H; RIKEN Plant Science Center, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan.; Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824, USA., Hubberten HM; Max Planck Institute of Molecular Plant Physiology, Am Mühlenberg 1, 14476 Potsdam-Golm, Germany., Hoefgen R; Max Planck Institute of Molecular Plant Physiology, Am Mühlenberg 1, 14476 Potsdam-Golm, Germany., Maruyama-Nakashita A; Faculty of Bioscience, Fukui Prefectural University, 4-1-1 Kenjojima, Matsuoka, Eiheiji-town, Fukui 910-1195, Japan.; RIKEN Plant Science Center, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan.; Graduate School of Agricultural Science, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan.
Jazyk: angličtina
Zdroj: Science advances [Sci Adv] 2016 Oct 07; Vol. 2 (10), pp. e1601087. Date of Electronic Publication: 2016 Oct 07 (Print Publication: 2016).
DOI: 10.1126/sciadv.1601087
Abstrakt: Glucosinolates (GSLs) in the plant order of the Brassicales are sulfur-rich secondary metabolites that harbor antipathogenic and antiherbivory plant-protective functions and have medicinal properties, such as carcinopreventive and antibiotic activities. Plants repress GSL biosynthesis upon sulfur deficiency (-S); hence, field performance and medicinal quality are impaired by inadequate sulfate supply. The molecular mechanism that links -S to GSL biosynthesis has remained understudied. We report here the identification of the -S marker genes sulfur deficiency induced 1 ( SDI1 ) and SDI2 acting as major repressors controlling GSL biosynthesis in Arabidopsis under -S condition. SDI1 and SDI2 expression negatively correlated with GSL biosynthesis in both transcript and metabolite levels. Principal components analysis of transcriptome data indicated that SDI1 regulates aliphatic GSL biosynthesis as part of -S response. SDI1 was localized to the nucleus and interacted with MYB28, a major transcription factor that promotes aliphatic GSL biosynthesis, in both yeast and plant cells. SDI1 inhibited the transcription of aliphatic GSL biosynthetic genes by maintaining the DNA binding composition in the form of an SDI1-MYB28 complex, leading to down-regulation of GSL biosynthesis and prioritization of sulfate usage for primary metabolites under sulfur-deprived conditions.
Databáze: MEDLINE
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