Cadmium-mediated toxicity in plant cells is associated with the DCD/NRP-mediated cell death response

Abstract

Cadmium (Cd²⁺ ) is highly harmful to plant growth. Although Cd²⁺ induces programmed cell death (PCD) in plant cells, Cd²⁺ stress in whole plants during later developmental stages and the mechanism underlying Cd²⁺ -mediated toxicity are poorly understood. Here, we showed that Cd²⁺ limits plant growth, causes intense redness in leaf vein, leaf yellowing, and chlorosis during the R1 reproductive stage of soybean (Glycine max). These symptoms were associated with Cd²⁺ -induced PCD, as Cd²⁺ -stressed soybean leaves displayed decreased number of nuclei, enhanced cell death, DNA damage, and caspase 1 activity compared to unstressed leaves. Accordingly, Cd²⁺ -induced NRPs, GmNAC81, GmNAC30 and VPE, the DCD/NRP-mediated cell death signalling components, which execute PCD via caspase 1-like VPE activity. Furthermore, overexpression of the positive regulator of this cell death signalling GmNAC81 enhanced sensitivity to Cd²⁺ stress and intensified the hallmarks of Cd²⁺ -mediated PCD. GmNAC81 overexpression enhanced Cd²⁺ -induced H₂ O₂ production, cell death, DNA damage, and caspase-1-like VPE expression. Conversely, BiP overexpression negatively regulated the NRPs/GmNACs/VPE signalling module, conferred tolerance to Cd²⁺ stress and reduced Cd²⁺ -mediated cell death. Collectively, our data indicate that Cd²⁺ induces PCD in plants via activation of the NRP/GmNAC/VPE regulatory circuit that links developmentally and stress-induced cell death.

Keywords: NAC; binding protein (BiP); cell death; soybean; vacuolar processing enzyme (VPE).