Sulfur deficiency-induced repressor proteins optimize glucosinolate biosynthesis in plants

Fayezeh Aarabi, Miyuki Kusajima, Takayuki Tohge, Tomokazu Konishi, Tamara Gigolashvili, Makiko Takamune, Yoko Sasazaki, Mutsumi Watanabe, Hideo Nakashita, Alisdair R. Fernie, Kazuki Saito, Hideki Takahashi, Hans Michael Hubberten, Rainer Hoefgen, Akiko Maruyama-Nakashita

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)

Abstract

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.2016

Original languageEnglish
Article numbere1601087
JournalScience Advances
Volume2
Issue number10
DOIs
Publication statusPublished - Oct 2016

All Science Journal Classification (ASJC) codes

  • General

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