Anthropogenic pollution of agricultural soils with cadmium (Cd) should receive adequate attention as Cd accumulation in crops endangers human health. When Cd is present in the soil, plants are exposed to it throughout their entire life cycle. As it is a non-essential element, no specific Cd uptake mechanisms are present. Therefore, Cd enters the plant through transporters for essential elements and consequently disturbs plant growth and development. In this review, we will focus on the effects of Cd on the most important events of a plant’s life cycle covering seed germination, the vegetative phase and the reproduction phase. Within the vegetative phase, the disturbance of the cell cycle by Cd is highlighted with special emphasis on endoreduplication, DNA damage and its relation to cell death. Furthermore, we will discuss the cell wall as an important structure in retaining Cd and the ability of plants to actively modify the cell wall to increase Cd tolerance. As Cd is known to affect concentrations of reactive oxygen species (ROS) and phytohormones, special emphasis is put on the involvement of these compounds in plant developmental processes. Lastly, possible future research areas are put forward and a general conclusion is drawn, revealing that Cd is agonizing for all stages of plant development.

Cadmium (Cd) exposure causes an oxidative challenge and inhibits cell cycle progression, ultimately impacting plant growth. Stress-induced effects on the cell cycle are often a consequence of activation of the DNA damage response (DDR). The main aim of this study was to investigate the role of the transcription factor SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1) and three downstream cyclin-dependent kinase inhibitors of the SIAMESE-RELATED (SMR) family in the Cd-induced DDR and oxidative challenge in leaves of Arabidopsis thaliana. Effects of Cd on plant growth, cell cycle regulation and the expression of DDR genes were highly similar between the wildtype and smr4/5/7 mutant. In contrast, sog1-7 mutant leaves displayed a much lower Cd sensitivity within the experimental time-frame and significantly less pronounced upregulations of DDR-related genes, indicating the involvement of SOG1 in the Cdinduced DDR. Cadmium-induced responses related to the oxidative challenge were disturbed in the sog1-7 mutant, as indicated by delayed Cd-induced increases of hydrogen peroxide and glutathione concentrations and lower upregulations of oxidative stress-related genes. In conclusion, our results attribute a novel role to SOG1 in regulating the oxidative stress response and connect oxidative stress to the DDR in Cd-exposed plants.

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Cadmium (Cd) uptake from polluted soils inhibits plant growth and disturbs physiological processes, at least partly due to disturbances in the cellular redox environment. Although the sulfur-containing antioxidant glutathione is important in maintaining redox homeostasis, its role as an antioxidant can be overruled by its involvement in Cd chelation as a phytochelatin precursor. Following Cd exposure, plants rapidly invest in phytochelatin production, thereby disturbing the redox environment by transiently depleting glutathione concentrations. Consequently, a network of signalling responses is initiated, in which the phytohormone ethylene is an important player involved in the recovery of glutathione levels. Furthermore, these responses are intricately connected to organellar stress signalling and autophagy and contribute to cell fate determination. In general, this may pave the way for acclimation (e.g. restoration of glutathione levels and organellar homeostasis) and plant tolerance in case of mild stress conditions. This review addresses connections between these players and discusses the possible involvement of the gasotransmitter hydrogen sulfide in plant acclimation to Cd exposure.

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