Sulfur deficiency-induced repressor proteins optimize glucosinolate biosynthesis in plants

Area of Science:

• Plant biochemistry
• Molecular biology
• Plant physiology

Background:

• Glucosinolates (GSLs) are sulfur-rich compounds in Brassicales plants, crucial for defense and medicinal properties.
• Plants suppress GSL biosynthesis under sulfur deficiency (-S), negatively impacting crop yield and quality.
• The molecular link between sulfur deficiency and GSL biosynthesis regulation is not well understood.

Purpose of the Study:

• To identify molecular regulators controlling glucosinolate biosynthesis under sulfur-limited conditions in Arabidopsis.
• To elucidate the mechanism by which sulfur deficiency represses GSL production.

Main Methods:

• Gene expression analysis of sulfur deficiency-induced genes (SDI1, SDI2).
• Metabolite profiling of glucosinolates.
• Transcriptome analysis using Principal Components Analysis (PCA).
• Yeast and plant cell-based interaction assays (co-localization, protein-protein interaction).

Main Results:

• Identified sulfur deficiency induced 1 (SDI1) and SDI2 as major repressors of GSL biosynthesis under -S.
• SDI1 and SDI2 expression negatively correlated with GSL biosynthesis at transcript and metabolite levels.
• SDI1 interacts with MYB28, a transcription factor promoting GSL biosynthesis, forming a complex that represses GSL biosynthetic genes.
• SDI1's nuclear localization and interaction with MYB28 inhibit GSL gene transcription, prioritizing sulfate for primary metabolism.

Conclusions:

• SDI1 and SDI2 are critical negative regulators of GSL biosynthesis in response to sulfur deficiency in Arabidopsis.
• The SDI1-MYB28 complex is a key molecular mechanism for repressing GSL production under low-sulfur conditions.
• Understanding this regulatory pathway is vital for improving crop performance and medicinal quality in Brassicales plants.