SummaryExperiments on Cd-contaminated soil demonstrated a contribution of phytochelatin synthesis to agriculturally relevant Cd accumulation and revealed constitutive activity of the hitherto functionally not understood Arabidopsis thaliana phytochelatin synthase2.
Lead (Pb) ranks first among metals with respect to tonnage produced and released into the environment. It is highly toxic and therefore an important pollutant of worldwide concern. Plant Pb uptake, accumulation, and detoxification mobilize Pb into food webs. Still, knowledge about the underlying mechanisms is very limited. This is largely due to serious experimental challenges with respect to Pb availability. In most studies, Pb(II) concentrations in the millimolar range have been used even though the toxicity threshold is in the nanomolar range. We therefore developed a low-phosphate, low-pH assay system that is more realistic with respect to soil solution conditions. In this system the growth of Arabidopsis thaliana seedlings was significantly affected by the addition of only 0.1 μM Pb(NO3)2. Involvement of phytochelatins in the detoxification of Pb(II) could be demonstrated by investigating phytochelatin synthase mutants. They showed a stronger inhibition of root growth and a lack of Pb-activated phytochelatin synthesis. In contrast, other putative Pb hypersensitive mutants were unaffected under these conditions, further supporting the essential role of phytochelatins for Pb detoxification. Our findings demonstrate the need to monitor plant Pb responses at realistic concentrations under controlled conditions and provide a strategy to achieve this.
Phytochelatin (PC) synthesis is essential for the detoxification of non-essential metals such as cadmium (Cd). In vitro experiments with Arabidopsis thaliana seedlings had indicated a contribution to zinc (Zn) tolerance as well. We addressed the physiological role of PC synthesis in Zn homeostasis of plants under more natural conditions. Growth responses, PC accumulation and leaf ionomes of wild-type and AtPCS1 mutant plants cultivated in different soils representing adequate Zn supply, Zn deficiency and Zn excess were analyzed. Growth on Zn-contaminated soil triggers PC synthesis and is strongly impaired in PC-deficient mutants. In fact, the contribution of AtPCS1 to tolerating Zn excess is comparable with that of the major Zn tolerance factor MTP1. For plants supplied with a normal level of Zn, a significant reduction in leaf Zn accumulation of AtPCS1 mutants was detected. In contrast, AtPCS1 mutants grown under Zn-limited conditions showed wild-type levels of Zn accumulation, suggesting the operation of distinct Zn translocation pathways. Contrasting phenotypes of the tested AtPCS1 mutant alleles upon growth in Zn- or Cd-contaminated soil indicated differential activation of PC synthesis by these metals. Experiments with truncated versions identified a part of the AtPCS1 protein required for the activation by Zn but not by Cd.
Phytochelatin synthases (PCS) play key roles in plant metal tolerance. They synthesize small metal-binding peptides, phytochelatins, under conditions of metal excess. Respective mutants are strongly cadmium and arsenic hypersensitive. However, their ubiquitous presence and constitutive expression had long suggested a more general function of PCS besides metal detoxification. Indeed, phytochelatin synthase1 from Arabidopsis thaliana (AtPCS1) was later implicated in non-host resistance. The two different physiological functions may be attributable to the two distinct catalytic activities demonstrated for AtPCS1, that is the dipeptidyl transfer onto an acceptor molecule in phytochelatin synthesis, and the proteolytic deglycylation of glutathione conjugates. In order to test this hypothesis and to possibly separate the two biological roles, we expressed a phylogenetically distant PCS from Caenorhabditis elegans in an AtPCS1 mutant. We confirmed the involvement of AtPCS1 in non-host resistance by showing that plants lacking the functional gene develop a strong cell death phenotype when inoculated with the potato pathogen Phytophthora infestans. Furthermore, we found that the C. elegans gene rescues phytochelatin synthesis and cadmium tolerance, but not the defect in non-host resistance. This strongly suggests that the second enzymatic function of AtPCS1, which remains to be defined in detail, is underlying the plant immunity function.
Thioarsenates form from arsenite under sulfate-reducing conditions, e.g., in rice paddy soils, and are structural analogues of arsenate. Even though rice is one of the most important sources of human arsenic intake, nothing is published about uptake, toxicity, or tolerance of thioarsenates in plants. Experiments using the model system Arabidopsis thaliana showed that monothioarsenate is less toxic than arsenite, but more toxic than arsenate at concentrations ≥25 μM As, reflected in stronger seedling growth inhibition on agar plates. Despite higher toxicity, total As accumulation in roots was lower upon exposure to monothioarsenate compared to arsenate, and a higher root efflux was confirmed. Root-shoot translocation was higher for monothioarsenate than for arsenate. Compared to the wild type (Col-0), both arsenate and monothioarsenate induced higher toxicity in phytochelatin (PC)-deficient mutants (cad1-3) as well as in glutathione biosynthesis (cad2) and PC transport (abcc12) mutants, demonstrating the important role of the PC pathway, not only for arsenate, but also for monothioarsenate detoxification. In Col-0, monothioarsenate induced relatively higher accumulation of PCs than arsenate. The observed differences in plant uptake, toxicity, and tolerance of thioarsenate vs oxyarsenate show that studying the effects of As on plants should include experiments with thiolated As species.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.