Heavy metal (HM) toxicity is one of the major abiotic stresses leading to hazardous effects in plants. A common consequence of HM toxicity is the excessive accumulation of reactive oxygen species (ROS) and methylglyoxal (MG), both of which can cause peroxidation of lipids, oxidation of protein, inactivation of enzymes, DNA damage and/or interact with other vital constituents of plant cells. Higher plants have evolved a sophisticated antioxidant defense system and a glyoxalase system to scavenge ROS and MG. In addition, HMs that enter the cell may be sequestered by amino acids, organic acids, glutathione (GSH), or by specific metal-binding ligands. Being a central molecule of both the antioxidant defense system and the glyoxalase system, GSH is involved in both direct and indirect control of ROS and MG and their reaction products in plant cells, thus protecting the plant from HM-induced oxidative damage. Recent plant molecular studies have shown that GSH by itself and its metabolizing enzymes—notably glutathione S-transferase, glutathione peroxidase, dehydroascorbate reductase, glutathione reductase, glyoxalase I and glyoxalase II—act additively and coordinately for efficient protection against ROS- and MG-induced damage in addition to detoxification, complexation, chelation and compartmentation of HMs. The aim of this review is to integrate a recent understanding of physiological and biochemical mechanisms of HM-induced plant stress response and tolerance based on the findings of current plant molecular biology research.

https://downloads.hindawi.com/archive/2012/872875.pdf

Molecular Mechanism of Heavy Metal Toxicity and Tolerance in Plants: Central Role of Glutathione in Detoxification of Reactive Oxygen Species and Methylglyoxal and in Heavy Metal Chelation

In mammals, cadmium is widely considered as a non-genotoxic carcinogen acting through a methylation-dependent epigenetic mechanism. Here, the effects of Cd treatment on the DNA methylation patten are examined together with its effect on chromatin reconfiguration in Posidonia oceanica. DNA methylation level and pattern were analysed in actively growing organs, under short- (6 h) and long- (2 d or 4 d) term and low (10 mM) and high (50 mM) doses of Cd, through a Methylation-Sensitive Amplification Polymorphism technique and an immunocytological approach, respectively. The expression of one member of the CHROMOMETHYLASE (CMT) family, a DNA methyltransferase, was also assessed by qRT-PCR. Nuclear chromatin ultrastructure was investigated by transmission electron microscopy. Cd treatment induced a DNA hypermethylation, as well as an up-regulation of CMT, indicating that de novo methylation did indeed occur. Moreover, a high dose of Cd led to a progressive heterochromatinization of interphase nuclei and apoptotic figures were also observed after long-term treatment. The data demonstrate that Cd perturbs the DNA methylation status through the involvement of a specific methyltransferase. Such changes are linked to nuclear chromatin reconfiguration likely to establish a new balance of expressed/repressed chromatin. Overall, the data show an epigenetic basis to the mechanism underlying Cd toxicity in plants.

/pdf/in-posidonia-oceanica-cadmium-induces-changes-in-dna-3cu7uj83mr.pdf

In Posidonia oceanica cadmium induces changes in DNA methylation and chromatin patterning

Heavy metals such as Fe, Mn, Cu, Ni, Co, Cd, Zn, Hg and arsenic are for long being accumulated in soils through industrial waste and sewage disposal. Although some of these metals are essential micronutrients responsible for many regular processes in plants, their excess, however, can have detrimental effects and can directly influence the plant growth, metabolism, physiology and senescence. Plants have different mechanisms to fight stress, and they are responsible to maintain homeostasis of essential metals required by plants. These mechanisms also focus on prevention of plants exposure to heavy metals present in the soil or providing tolerance to the plant by detoxifying the metals. Other mechanisms are specific and are initiated when the respective stress is encountered. The first line of defense provided by a plant is to reduce the uptake of metals when stimulated with toxicity of heavy metals and includes the help offered by cellular and root exudates that restricts metals from entering the cell. Many plants have exclusive mechanisms for individual metal ions and are involved in sequestering these ions in compartments avoiding their exposure to sensitive components of the cells. As a second line of defense, other mechanisms for detoxification of these metals are introduced that chelates, transports, sequesters and detoxifies these metal ions in the plant’s vacuole. During the time of metal toxicity, oxidative stress is pronounced in the cells and production of stress-related proteins and hormones, antioxidants, signaling molecules including heat-shock proteins synthesis is initiated.

Heavy metal stress and responses in plants

Plants respond to environmental pollutants such as heavy metal(s) by triggering the expression of genes that encode proteins involved in stress response. Toxic metal ions profoundly affect the cellular protein homeostasis by interfering with the folding process and aggregation of nascent or non-native proteins leading to decreased cell viability. However, plants possess a range of ubiquitous cellular surveillance systems that enable them to efficiently detoxify heavy metals towards enhanced tolerance to metal stress. As proteins constitute the major workhorses of living cells, the chelation of metal ions in cytosol with phytochelatins and metallothioneins followed by compartmentalization of metals in the vacuoles as well as the repair of stress-damaged proteins or removal and degradation of proteins that fail to achieve their native conformations are critical for plant tolerance to heavy metal stress. In this review, we provide a broad overview of recent advances in cellular protein research with regards to heavy metal tolerance in plants. We also discuss how plants maintain functional and healthy proteomes for survival under such capricious surroundings.

/pdf/responses-of-plant-proteins-to-heavy-metal-stress-a-review-45mlvebcqm.pdf

Responses of Plant Proteins to Heavy Metal Stress—A Review

Plant proteomics update (2007-2008) : Second-generation proteomic techniques, an appropriate experimental design, and data analysis to fulfill MIAPE standards, increase plant proteome coverage and expand biological knowledge

Phytotoxic aluminum (Al) is a limiting factor for crop production on acid soils. The molecular mechanism, however, underlying Al toxicity and responses in plants is still not well understood. We report here the characterization of comparative proteome of aluminum-stress-responsive proteins in a known Al-resistant soybean cultivar, Baxi 10 (BX10). To investigate time-dependent responses, 1-week-old soybean seedlings were exposed to 50 microM AlCl3 for 24, 48 and 72 h, and total proteins extracted from roots were separated by two-dimensional electrophoresis. More than 1200 root proteins of the soybean BX10 seedling were reproducibly resolved on the gels. A total of 39 differentially expressed spots in abundance were identified by mass spectrometry, with 21 upregulated, 13 newly induced and 5 downregulated. The heat shock protein, glutathione S-transferase, chalcone-related synthetase, GTP-binding protein and ABC transporter ATP-binding protein were previously detected at the transcriptional or translational level in other plants. Other proteins, identified in this study, are new Al-induced proteins. Soybean BX10 roots under aluminum stress could be characterized by the cellular activities involved in stress/defense, signal transduction, transport, protein folding, gene regulation, and primary metabolisms, which are critical for plant survival under Al toxicity. This present study expands our understanding of differentially expressed proteins associated with aluminum stress on soybean BX10.

Comparative proteome analysis of differentially expressed proteins induced by Al toxicity in soybean.

Seedlings of two soybean genotypes, BX10 [aluminum (Al)-tolerant] and BD2 (Al-sensitive), were treated with Al to evaluate the relative root growth (RRG), callose content, Al-sensitive zone, lipid peroxidation, and the anti-oxidative enzyme activities by histochemical and biochemical assays. Under Al toxicity, the RRG reduction of BD2 was more significant than that of BX10, while callose content displayed a contrary trend. The 2–5 mm zone of root apex was the main Al-sensitive zone for soybeans. The activities of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and ascorbate peroxidase (APX) were found to be higher in the two genotypes under Al toxicity than that of the controls. The SOD, POD, and CAT activities of BX10; however, were significantly lower than those of BD2. These results implied that producing low quantity of ROS may be one aspect of the Al-tolerant mechanism for soybeans, which in turn helps them adapt to Al stress.

Lv Miao

Papers

Comparative proteome analysis of differentially expressed proteins induced by Al toxicity in soybean.

Differential responses of anti-oxidative enzymes to aluminum stress in tolerant and sensitive soybean genotypes.