Cadmium (Cd) contamination presents a grave threat to the growth and development of plants. One of its fundamental toxicological mechanisms is the disruption of cellular redox homeostasis. To clarify the physiological and molecular mechanisms through which Cerasus humilis responds to Cd stress, this study utilized physiological and biochemical analyses, transcriptomics, and transgenic functional validation methods. The results demonstrate that Cd stress leads to a substantial buildup of reactive oxygen species (ROS) and intensifies membrane lipid peroxidation in C. humilis leaves. This is evidenced by significant elevations in superoxide anion (O₂ ⁻), hydrogen peroxide (H₂O₂), and malondialdehyde (MDA) levels. Transcriptome analysis pinpointed a crucial response factor, ChERF017. Heterologous overexpression of this gene in Arabidopsis thaliana significantly enhanced the tolerance to Cd stress, which was manifested as follows: under the stress of 100 µmol/L CdCl₂, the transgenic line displayed less severe chlorophyll degradation, the levels of ROS accumulation were notably reduced, the activity of antioxidant enzymes increased, and the content of glutathione and phytochelatins (PCs) increased. This promoted the transport of free Cd into vacuoles, thereby alleviating their cytotoxic effects on cells. This study verifies that ChERF017 plays a vital role in plant tolerance to Cd by regulating the antioxidant enzyme system and influencing the distribution of Cd within the cell. This finding offers essential theoretical bases and genetic resources for the genetic improvement of Cd resistance in C. humilis. The transcription factor ChERF017 positively regulates cadmium stress response in Cerasus humilis via the antioxidant pathway.
Ji et al. (Sat,) studied this question.