Cadmium‐mediated toxicity in plant cells is associated with the DCD/NRP‐mediated cell death response
Iana Pedro Silva Quadros, Nayara Nolasco Madeira, Virgílio A. P. Loriato, Thaina Fernanda Fillietaz Saia, Jéssica Coutinho Silva, Fernanda Aparecida Ferrari Soares, José Romário de Carvalho, Pedro A. B. Reis, Elizabeth P. B. Fontes, Wellington Ronildo Clarindo, Renildes Lúcio Ferreira Fontes
Abstract
Abstract Cadmium (Cd 2+ ) is highly harmful to plant growth. Although Cd 2+ induces programmed cell death (PCD) in plant cells, Cd 2+ stress in whole plants during later developmental stages and the mechanism underlying Cd 2+ ‐mediated toxicity are poorly understood. Here, we showed that Cd 2+ 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 Cd 2+ ‐induced PCD, as Cd 2+ ‐stressed soybean leaves displayed decreased number of nuclei, enhanced cell death, DNA damage, and caspase 1 activity compared to unstressed leaves. Accordingly, Cd 2+ ‐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 Cd 2+ stress and intensified the hallmarks of Cd 2+ ‐mediated PCD. GmNAC81 overexpression enhanced Cd 2+ ‐induced H 2 O 2 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 Cd 2+ stress and reduced Cd 2+ ‐mediated cell death. Collectively, our data indicate that Cd 2+ induces PCD in plants via activation of the NRP/GmNAC/VPE regulatory circuit that links developmentally and stress‐induced cell death.