Cadmium (Cd) is non-essential heavy metal, which in excess, exhibits deleterious effects to the most of the organisms. Mobilization of defense mechanisms against this toxic agent requires rapid activation of signaling pathways. The article presents recent advances in the research concerning cadmium signal transduction in plants. New insights into the involvement of reactive oxygen species, nitric oxide, plant growth regulators and Cd-induced protein modifications are reviewed. Moreover, the role of recently recognized Cd-associated signal elements, including micro RNAs and several cis- and trans- acting elements is discussed.
Pollution of the environment with plastic is an important concern of the modern world. It is estimated that annually over 350 million tonnes of this material are produced, wherein, despite the recycling methods, a significant part is deposited in the environment. The plastic has been detected in the industrial areas, as well as farmlands and gardens in many world regions. Larger plastic pieces degraded in time into smaller pieces including microplastic (MP) and nanoplastic particles (NP). Nanoplastic is suggested to pose the most serious danger as due to the small size, it is effectively taken up from the environment by the biota and transported within the organisms. An increasing number of reports show that NP exert toxic effects also on plants. One of the most common plant response to abiotic stress factors is the accumulation of reactive oxygen species (ROS). On the one hand, these molecules are engaged in cellular signalling and regulation of genes expression. On the other hand, ROS in excess lead to oxidation and damage of various cellular compounds. This article reviews the impact of NP on plants, with special emphasis on the oxidative response.
Increase in the level of reactive oxygen species (ROS) is a common response to stress factors, including exposure to metals. ROS over-production is associated with oxidation of lipids, proteins, and nucleic acids. It is suggested that the products of oxidation are not solely the markers of oxidative stress but also signaling elements. For instance, it has been shown in animal models that mRNA oxidation is a selective process engaged in post-transcriptional regulation of genes expression and that it is associated with the development of symptoms of several neurodegenerative disorders. In the present study, we examined the impact of short-term cadmium (Cd) stress on the level of two RNA oxidation markers: 8-hydroxyguanosine (8-OHG) and apurinic/apyrimidinic sites (AP-sites, abasic sites). In the case of 8-OHG, a significant increase was observed after 3 h of exposure to moderate Cd concentration (10 mg/l). In turn, high level of AP-sites, accompanied by strong ROS accumulation and lipid peroxidation, was noted only after 24 h of treatment with higher Cd concentration (25 mg/l). This is the first report showing induction of RNA oxidations in plants response to stress factors. The possible signaling and gene regulatory role of oxidatively modified transcripts is discussed.
The phenomenon of cross-resistance allows plants to acquire resistance to a broad range of stresses after previous exposure to one specific factor. Although this stress–response relationship has been known for decades, the sequence of events that underpin cross-resistance remains unknown. Our experiments revealed that susceptible potato (Solanum tuberosum L. cv. Bintje) undergoing aluminum (Al) stress at the root level showed enhanced defense responses correlated with reduced disease symptoms after leaf inoculation with Phytophthora infestans. The protection capacity of Al to subsequent stress was associated with the local accumulation of H2O2 in roots and systemic activation of salicylic acid (SA) and nitric oxide (NO) dependent pathways. The most crucial Al-mediated changes involved coding of NO message in an enhanced S-nitrosothiol formation in leaves tuned with an abundant SNOs accumulation in the main vein of leaves. Al-induced distal NO generation was correlated with the overexpression of PR-2 and PR-3 at both mRNA and protein activity levels. In turn, after contact with a pathogen we observed early up-regulation of SA-mediated defense genes, e.g. PR1, PR-2, PR-3 and PAL, and subsequent disease limitation. Taken together Al exposure induced distal changes in the biochemical stress imprint, facilitating more effective responses to a subsequent pathogen attack.