Cadmium (Cd) is an environmentally polluted toxic heavy metal and seriously risks food safety and human health through food chain. Mining genetic potentials of plants is a crucial step for limiting Cd accumulation in rice crops and improving environmental quality. This study characterized a novel locus in rice genome encoding a Cd-binding protein named OsHIPP16, which resides in the nucleus and near plasma membrane. OsHIPP16 was strongly induced by Cd stress. Histochemical analysis with pHIPP16::GUS reveals that OsHIPP16 is primarily expressed in root and leaf vascular tissues. Expression of OsHIPP16 in the yeast mutant strain ycf1 sensitive to Cd conferred cellular tolerance. Transgenic rice overexpressing OsHIPP16 (OE) improved rice growth with increased plant height, biomass, and chlorophyll content but with a lower degree of oxidative injury and Cd accumulation, whereas knocking out OsHIPP16 by CRISPR-Cas9 compromised the growth and physiological response. A lifelong trial with Cd-polluted soil shows that the OE plants accumulated much less Cd, particularly in brown rice where the Cd concentrations declined by 11.76–34.64%. Conversely, the knockout oshipp16 mutants had higher levels of Cd with the concentration in leaves being increased by 26.36–35.23% over the wild-type. These results suggest that adequate expression of OsHIPP16 would profoundly contribute to Cd detoxification by regulating Cd accumulation in rice, suggesting that both OE and oshipp16 mutant plants have great potentials for restricting Cd acquisition in the rice crop and phytoremediation of Cd-contaminated wetland soils.

Heavy metal toxicity has become an impediment to agricultural productivity, which presents major human health concerns in terms of food safety. Among them, arsenic (As) a non-essential heavy metal has gained worldwide attention because of its noxious effects on agriculture and public health. The increasing rate of global warming and anthropogenic activities have promptly exacerbated As levels in the agricultural soil, thereby causing adverse effects to crop genetic and phenotypic traits and rendering them vulnerable to other stresses. Conventional breeding and transgenic approaches have been widely adapted for producing heavy metal resilient crops; however, they are time-consuming and labor-intensive. Hence, finding new mitigation strategies for As toxicity would be a game-changer for sustainable agriculture. One such promising approach is harnessing plant microbiome in the era of ‘omics’ which is gaining prominence in recent years. The use of plant microbiome and their cocktails to combat As metal toxicity has gained widespread attention, because of their ability to metabolize toxic elements and offer an array of perquisites to host plants such as increased nutrient availability, stress resilience, soil fertility, and yield. A comprehensive understanding of below-ground plant-microbiome interactions and their underlying molecular mechanisms in exhibiting resilience towards As toxicity will help in identifying elite microbial communities for As mitigation. In this review, we have discussed the effect of As, their accumulation, transportation, signaling, and detoxification in plants. We have also discussed the role of the plant microbiome in mitigating As toxicity which has become an intriguing research frontier in phytoremediation. This review also provides insights on the advancements in constructing the beneficial synthetic microbial communities (SynComs) using microbiome engineering that will facilitate the development of the most advanced As remedial tool kit in sustainable agriculture.

Azoxystrobin (AZ) and pyraclostrobin (PY) are strobilurin fungicides that inhibit fungal mitochondrial respiration. In this study, a representative model, zebrafish (Danio rerio), was used as a test species for acute and developmental toxicity. Survival and malformation rates were observed only PY-treated embryos, with an LC₅₀ value of 77.75 ppb accompanied by a dramatic decrease in hatching rate, while AZ did not show great mortality. Morphological changes were observed in PY-treated embryos with the occurrence of pericadial edema at 25 ppb. A delay in growth was observed after treatment with pyraclostrobin at 50 ppb. Use of genetically engineered Tg(cmlc:EGFP) allowed fluorescence observation during heart development. PY interfered with normal heart development via upregulation of the nppa gene responsible for the expression of natriuretic peptides. Heart function was dramatically reduced as indicated by reduced heart rates. Increased expression of the nppa gene was also seen in AZ-treated embryos. The expression level of cyp24a1 was also up-regulated, while ugt1a1 and sult1st6 were down-regulated after treatment of zebrafish embryos with AZ or PY. Overall, strobilurin fungicides might inhibit normal heart formation and function within the range of concentrations tested.

Increasing attention has been brought to microplastics pollution recently, while emerging evidences indicate that nano-plastics degraded from microplastics are more of research significance owing to stronger toxicity. However, there is little study focused on the prevention of nano-plastics induced toxicity until now. Canidin-3-glucoside (C3G), a natural anthocyanin proved to possess multiple functions like antioxidant and intestinal tissue protection. Thus, we proposed whether C3G could act as a molecular weapon against nano-plastics induced toxicity. In Caco2 cell and Caenorhabditis elegans (C. elegans) models, we found that polystyrene (PS) nano-plastics exposure resulted in physiological toxicity and oxidative damage, which could be restored by C3G. More significantly in Caco2 cells, we observed that autophagy was activated via Sirt1-Foxo1 signaling pathway to attenuate PS induced toxicity after C3G intervention and further verified by adding autophagy inhibitor 3-Methyladenine (3-MA). Meanwhile, PS co-localization with lysosomes was observed, indicating the encapsulation and degradation of PS. In C. elegans, by detecting LGG-1/LC3 expression in GFP-targeted LGG-1 report gene (LGG-1:GFP) labeled transgenic DA2123 strain, the co-localization of LGG-1:GFP with PS was found as well, means that autophagy is involved in C3G’s beneficial effects. Furthermore, we were surprised to find that C3G could promote the discharge of PS from N2 nematodes, which reduces PS toxicity more directly.

Triclosan (TCS) is an organic compound with a wide range of antibiotic activity and has been widely used in items ranging from hygiene products to cosmetics; however, recent studies suggest that it has several adverse effects. In particular, TCS can be passed to both fetus and infants, and while some evidence suggests in vitro neurotoxicity, there are currently few studies concerning the mechanisms of TCS-induced developmental neurotoxicity. Therefore, this study aimed to clarify the effect of TCS on neural development using zebrafish models, by analyzing the morphological changes, the alterations observed in fluorescence using HuC-GFP and Olig2-dsRED transgenic zebrafish models, and neurodevelopmental gene expression. TCS exposure decreased the body length, head size, and eye size in a concentration-dependent manner in zebrafish embryos. It increased apoptosis in the central nervous system (CNS) and particularly affected the structure of the CNS, resulting in decreased synaptic density and shortened axon length. In addition, it significantly up-regulated the expression of genes related to axon extension and synapse formation such as α1-Tubulin and Gap43, while decreasing Gfap and Mbp related to axon guidance, myelination and maintenance. Collectively, these changes indicate that exposure to TCS during neurodevelopment, especially during axonogenesis, is toxic. This is the first study to demonstrate the toxicity of TCS during neurogenesis, and suggests a possible mechanism underlying the neurotoxic effects of TCS in developing vertebrates.

Antibiotic resistance genes may be considered as environmental pollutants if anthropogenic emission and manipulations increase their prevalence above usually occurring background levels. The prevalence of aph(3′)-IIa/nptII and aph(3′)-IIIa/nptIII – frequent marker genes in plant biotechnology conferring resistance to certain aminoglycosides – was determined in Austrian soils from 100 maize and potato fields not yet exposed to but eligible for GMO crop cultivation. Total soil DNA extracts were analysed by nptII/nptIII-specific TaqMan real time PCR. Of all fields 6% were positive for nptII (median: 150 copies/g soil; range: 31–856) and 85% for nptIII (1190 copies/g soil; 13–61600). The copy-number deduced prevalence of nptIII carriers was 14-fold higher compared to nptII. Of the cultivable kanamycin-resistant soil bacteria 1.8% (95% confidence interval: 0–3.3%) were positive for nptIII, none for nptII (0–0.8%). The nptII-load of the studied soils was low rendering nptII a typical candidate as environmental pollutant upon anthropogenic release into these ecosystems.

Tropospheric ozone concentrations have been rising across Asia, and will continue to rise during the 21st century. Ozone affects rice yields through reductions in spikelet number, spikelet fertility, and grain size. Moreover, ozone leads to changes in rice grain and straw quality. Therefore the breeding of ozone tolerant rice varieties is warranted. The mapping of quantitative trait loci (QTL) using bi-parental populations identified several tolerance QTL mitigating symptom formation, grain yield losses, or the degradation of straw quality. A genome-wide association study (GWAS) demonstrated substantial natural genotypic variation in ozone tolerance in rice, and revealed that the genetic architecture of ozone tolerance in rice is dominated by multiple medium and small effect loci. Transgenic approaches targeting tolerance mechanisms such as antioxidant capacity are also discussed. It is concluded that the breeding of ozone tolerant rice can contribute substantially to the global food security, and is feasible using different breeding approaches.

Insufficient evidence exists regarding the effects of microplastics (MPs) on the neuronal toxicity of heavy metals in the early stages of organisms. Herein, the effects of micro-polystyrene (μ-PS; 157 μm) and nano-polystyrene (n-PS; 100 nm) particles on the neurodevelopmental toxicity of mercury (Hg) in zebrafish embryos were compared. Zebrafish embryos exposed to Hg at the concentration of 0.1 mg L⁻¹ revealed blood disorders, delayed hatching, and malformations such as pericardial oedema and tail deformity. The length of the larval head was significantly reduced (P < 0.01) and in vivo expression of atoh1a in the cerebellum of neuron-specific transgenic zebrafish Tg(atoh1a:dTomato) larvae was inhibited by 29.46% under the Hg treatment. Most of the toxic effects were inhibited by the combined exposure to μ-PS or n-PS with Hg, and n-PS decreased the neurodevelopmental toxicity of Hg more significantly than μ-PS. Metabolomic analysis revealed that in addition to inhibiting the amino acid metabolism pathway as in the μ-PS+Hg treatment, the n-PS+Hg treatment inhibited unsaturated fatty acid metabolism in zebrafish larvae, likely because of a greater reduction in Hg bioavailability, thus reducing the oxidative damage caused by Hg in the larvae. The combined effects of MPs and heavy metals differ greatly among different species and their targeted effects. We conclude that the combined toxicity mechanisms of MPs and heavy metals require further clarification.

Cadmium (Cd) is a toxic heavy metal that initiates diverse chronic diseases through food chains. Developing a biotechnology for manipulating Cd uptake in plants is beneficial to reduce environmental and health risks. Here, we identified a novel epigenetic mechanism underlying Cd accumulation regulated by an uncharacterized metallochaperone namely Heavy Metal Responsive Protein (HMP) in rice plants. OsHMP resides in cytoplasm and nucleus, dominantly induced by Cd stress and binds directly to Cd ions. OsHMP overexpression enhanced the rice growth under Cd stress but accumulated more Cd, whereas knockout or knockdown of OsHMP showed a contrasting effect. The enhanced Cd accumulation in the transgenic lines was confirmed by a long-term experiment with rice growing at the environmentally realistic Cd concentration in soil. The bisulfite sequencing and chromatin immunoprecipitation assessments revealed that Cd stress reduced significantly the DNA methylation at CpG (Cytosine-Guanine) and histone H3K9me2 marks in the upstream of OsHMP. By identifying a couple of mutants defective in DNA methylation and histone modification (H3K9me2) such as Osmet1 (methylatransfease1) and Ossdg714 (kryptonite), we found that the Cd-induced epigenetic hypomethylation at the region was associated with OsHMP overexpression, which consequently led to Cd detoxification in rice. The causal relationship was confirmed by the GUS reporter gene coupled with OsHMP and OsMET1 whereby OsMET1 repressed directly the OsHMP expression. Our work signifies that expression of OsHMP is required for Cd detoxification in rice plants, and the Cd-induced hypomethylation in the specific region is responsible for the enhanced OsHMP expression. In summary, this study gained an insight into the epigenetic mechanism for additional OsHMP expression which consequently ensures rice adaptation to the Cd-contaminated environment.

2,2′,4,4′-Tetrabromodiphenyl ether (BDE-47), a representative congener of polybrominated diphenyl ethers in the environment, is known to have reproductive toxicity. However, the underlying mechanisms remain to be clarified, especially in in vivo systems. In the present study, we employed Caenorhabditis elegans to study the effects of BDE-47 on reproduction. Our results showed that BDE-47 impaired worm fecundity and induced germ cell apoptosis. To elucidate the mechanisms, DNA damage and oxidative stress induction were investigated by determining the numbers of foci formation in transgenic worms expressing HUS-1::GFP and the levels of reactive oxygen species, respectively. We found that BDE-47 induced oxidative stress but not DNA damage, and treatment with the antioxidant, N-acetyl-L-cysteine, completely abrogated BDE-47-induced germ cell apoptosis. In addition, the apoptosis was blocked in mutants carrying mek-1, sek-1 or abl-1 loss-of-function alleles, but not in the p53/cep-1 deficient worms, suggesting that the mitogen-activated protein kinase (MAPK) signaling cascade was essential for BDE-47-induced germ cell apoptosis and p53/cep-1 was not required. Moreover, the apoptosis in the strains deficient for DNA damage response was not suppressed under BDE-47 treatment. Overall, we demonstrated that BDE-47 could induce oxidative stress and subsequent germ cell apoptosis in Caenorhabditis elegans through a MAPK-mediated p53-independent pathway.