Abstract

Arsenic is a metalloid that is toxic to plants. Arsenate (As(V)), the prevalent chemical form of arsenic, is a phosphate (Pi) analog and is incorporated into plant cells via Pi transporters. Here, we found that the MYB40 transcription factor played important roles in the control of Arabidopsis As(V) resistance. The expression of MYB40 was induced by As(V) stress. MYB40-overexpressing lines had an obvious As(V)-resistant phenotype and a reduced As(V)/Pi uptake rate, whereas myb40 mutants were sensitive to As(V) stress. Upon exposure to As(V), MYB40 directly repressed the expression of PHT1;1, which encodes a main Pi transporter. The As(V)-resistant phenotypes of MYB40-overexpressing lines were impaired by overexpression of PHT1;1, demonstrating an epistatic genetic relationship between MYB40 and PHT1;1. Moreover, overexpression of MYB40 enhanced, and disruption of MYB40 reduced, thiol-peptide contents. Upon exposure to As(V), MYB40 positively regulated the expression of PCS1, which encodes a phytochelatin synthase, and ABCC1 and ABCC2, which encode the major vacuolar phytochelatin transporters. Together, our data demonstrate that AtMYB40 acts as a central regulator of As(V) responses, providing a genetic strategy for enhancing plant As(V) tolerance and reducing As(V) uptake to improve food safety.

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