Boron toxicity induces sulfate transporters at transcriptional level in Arabidopsis thaliana

Kayihan, Ceyhun
Aksoy, Emre
Mutlu, Su Naz
Plants activate glutathione (GSH)-dependent detoxification pathways at biochemical and molecular levels under boron (B) toxicity. Sulfate uptake and transport are necessary for GSH biosynthesis in plants. Therefore, the transcriptional regulation of some sulfate transporters was determined in this study to clarify the importance of these transporters in leaf and root tissues of Arabidopsis thaliana under toxic B conditions. The expression level of SULTR1;3 was dramatically increased in leaf and root tissues under moderate and severe toxic B conditions, suggesting source-to-sink sulfate translocation under B toxicity. Stable expression levels of SULTR2;1, SULTR2;2, and low SULTR3;5 expression might restrict the sulfate movement into the xylem in leaves. SULTR3;1, SULTR3;2, SULTR3;3, SULTR3;4, SULTR4;1 and SULTR4;2 were induced in root tissues under toxic B conditions, indicating an induction of root-to-shoot sulfate translocation. These results showed that B toxicity might disrupt the homogeneous distribution of sulfate and sulfur-containing compounds in both tissues of A. thaliana. Moreover, we performed in silico analysis of microarray experiments to determine the common differentially expressed genes (DEGs) under B toxicity and sulfur deficiency. Gene ontology, hierarchical clustering, and coexpression network analyses of these DEGs demonstrated the requirement of sulfate transporters under B toxicity. A set of genes involved in sulfur metabolism coexpress with sulfate transporters under B toxicity. To the best of our knowledge, this is the first report focusing on the molecular regulation of sulfate transporters in Arabidopsis thaliana under B toxicity.
Turkish Journal of Botany


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Citation Formats
C. Kayihan, E. Aksoy, and S. N. Mutlu, “Boron toxicity induces sulfate transporters at transcriptional level in Arabidopsis thaliana,” Turkish Journal of Botany, vol. 47, no. 1, pp. 0–0, 2023, Accessed: 00, 2023. [Online]. Available: