Understanding of aquaporins (AQPs) facilitating the transport of water and many other small solutes including metalloids like silicon (Si) and arsenic (As) is important to develop stress tolerant cultivars. In the present study, 40 AQPs were identified in the genome of pigeonpea (Cajanus cajan), a pulse crop widely grown in semi-arid region and areas known to affected with heavy metals like As. Conserved domains, variation at NPA motifs, aromatic/arginine (ar/R) selectivity filters, and pore morphology defined here will be crucial in predicting solute specificity of pigeonpea AQPs. The study identified CcNIP2-1 as an AQP predicted to transporter Si (beneficial element) as well as As (hazardous element). Further Si quantification in different tissues showed about 1.66% Si in leaves which confirmed the predictions. Furthermore, scanning electron microscopy showed a higher level of Si accumulation in trichomes on the leaf surface. A significant alleviation in level of As, Sb and Ge stress was also observed when these heavy metals were supplemented with Si. Estimation of relative water content, H₂O₂, lipid peroxidation, proline, total chlorophyll content and other physiological parameters suggested Si derived stress tolerance. Extensive transcriptome profiling under different developmental stages from germination to senescence was performed to understand the tissue-specific regulation of different AQPs. For instance, high expression of TIP3s was observed only in reproductive tissues. Co-expression network developed using transcriptome data from 30 different conditions and tissues, showed interdependency of AQPs. Expression profiling of pigeonpea performed using real time PCR showed differential expression of AQPs after Si supplementation. The information generated about the phylogeny, distribution, molecular evolution, solute specificity, and gene expression dynamics in article will be helpful to better understand the AQP transport system in pigeonpea and other legumes.

The intensification of anomalous events of seawater warming and the co-occurrence with local anthropogenic stressors are threatening coastal marine habitats, including seagrasses, which form extensive underwater meadows. Eutrophication highly affects coastal environments, potentially summing up to the widespread effects of global climate changes. In the present study, we investigated for the first time in seagrasses, the transcriptional response of different plant organs (i.e., leaf and shoot apical meristem, SAM) of the Mediterranean seagrass Posidonia oceanica growing in environments with a different history of nutrient enrichment. To this end, a mesocosm experiment exposing plants to single (nutrient enrichment or temperature increase) and multiple stressors (nutrient enrichment plus temperature increase), was performed. Results revealed a differential transcriptome regulation of plants under single and multiple stressors, showing an organ-specific sensitivity depending on plants' origin. While leaf tissues were more responsive to nutrient stress, SAM revealed a higher sensitivity to temperature treatments, especially in plants already impacted in their native environment. The exposure to stress conditions induced the modulation of different biological processes. Plants living in an oligotrophic environment were more responsive to nutrients compared to plants from a eutrophic environment. Evidences that epigenetic mechanisms were involved in the regulation of transcriptional reprogramming were also observed in both plants’ organs. These results represent a further step in the comprehension of seagrass response to abiotic stressors pointing out the importance of local pressures in a global warming scenario.

Perfluorooctanesulfonic acid (PFOS) is a persistent anthropogenic chemical that can affect the thyroid hormone system in humans and animals. In adults, thyroid hormones (THs) are regulated by the hypothalamic-pituitary-thyroid (HPT) axis, but also by organs such as the liver and potentially the gut microbiota. PFOS and other xenobiotics can therefore disrupt the TH system at various locations and through different mechanisms. To start addressing this, we exposed adult male rats to 3 mg PFOS/kg/day for 7 days and analysed effects on multiple organs and pathways simultaneously by transcriptomics. This included four primary organs involved in TH regulation, namely hypothalamus, pituitary, thyroid, and liver. To investigate a potential role of the gut microbiota in thyroid hormone regulation, two additional groups of animals were dosed with the antibiotic vancomycin (8 mg/kg/day), either with or without PFOS. PFOS exposure decreased thyroxine (T4) and triiodothyronine (T3) without affecting thyroid stimulating hormone (TSH), resembling a state of hypothyroxinemia. PFOS exposure resulted in 50 differentially expressed genes (DEGs) in the hypothalamus, 68 DEGs in the pituitary, 71 DEGs in the thyroid, and 181 DEGs in the liver. A concomitant compromised gut microbiota did not significantly change effects of PFOS exposure. Organ-specific DEGs did not align with TH regulating genes; however, genes associated with vesicle transport and neuronal signaling were affected in the hypothalamus, and phase I and phase II metabolism in the liver. This suggests that a decrease in systemic TH levels may activate the expression of factors altering trafficking, metabolism and excretion of TH. At the transcriptional level, little evidence suggests that the pituitary or thyroid gland is involved in PFOS-induced TH system disruption.

With the continued increase of global ammonia emission, the damage to human or animal caused by ammonia pollution has attracted wide attention. The noncoding RNAs have been reported to regulate a variety of biological processes under different environmental stimulation via ceRNA (competing endogenous RNA) networks. Autophagy is a hallmark of tissue damage from air pollution. However, the specific role of circular RNAs (circRNAs) in the injury of intestinal tissue caused by autophagy remains unclear. Here, we established 42-days old ammonia-exposed broiler models and observed that autophagy flux in broiler jejunum was activated under ammonia exposure. Meanwhile, a total of eight significantly dysregulated expressed circRNAs were obtained and a circRNAs-miRNAs-genes interaction networks were constructed by bioinformatics analysis. Furthermore, an axis named circRNA-IGLL1/miR-15a/RNF43 was predicted to participate in the excessive autophagy by targeting RNF43. The target relationship was proved by dual-luciferase reporter assay in vitro. Mechanistically, downregulated circRNA-IGLL1 could suppress the expression of RNF43 in ammonia-exposed jejunum and the Wnt/β-catenin pathway was activated. Inhibition of miR-15a reversed autophagy caused by downregulated circRNA-IGLL1. CircRNA-IGLL1 could competitively bind miR-15a to regulate RNF43 expression, thus modulating the occurrence of autophagy. Taken together, our results showed that circRNA-IGLL1/miR-15a/RNF43 axis is involved in ammonia-induced intestinal autophagy in broilers.

Tire particles pose a potential threat to terrestrial organisms because they are deposited in large quantities in the soil by tire wear abrasion, and moreover their chemical complexity poses an additional risk. Microplastics can affect several physiological processes in organisms, including those related to immunity. Therefore, we investigated the expression profile of selected immune-related genes (MnSod, Manganese Superoxide dismutase; Cat, Catalase; CypG, Cyclophilin G; Nos, Nitric oxide synthase; Ppae2a, Prophenoloxidase-activating enzyme 2a; Dscam, Down syndrome cell adhesion molecule; Myd88, Myeloid-differentiation factor 88; Toll4, Toll-like receptor 4; Mas-like, Masquerade-like protein) in haemocytes and the digestive gland hepatopancreas of terrestrial crustacean Porcellio scaber after two different time exposures (4 and 14 days) to tire particles in soil. Our results reveal for the first time the response of P. scaber after microplastic exposure at the transcriptome level. We observed time- and tissue-dependent changes in the expression of the analysed genes, with more pronounced alterations in haemocytes after 14 days of exposure. Some minor changes were also observed in hepatopancreas after 4 days. Changes in the expression profile of the analysed genes are a direct indication of a modulated immune status of the test organism, which, however, does not represent an adverse effect on the test organism under the given conditions. Nevertheless, the question remains whether the observed change in immune status affects the immunocompetence of the test organism.

As a widely used pure elemental carbon in colloidal particles, carbon black was listed as a group 2B carcinogen by IARC in 2010. The most available mechanism information about carbon black and carcinogenesis are from in vivo or in vitro studies. However, few studies concerned the nanoparticle's real-ambient exposure causing systemic change and further affecting the target organ. Herein, we used an ex vivo biosensor assay to investigate the transcriptome change of primary bronchial epithelial cells after treatment with the plasma from workers with long-term occupational carbon black exposure history. Based on ex vivo biosensor assay and transcriptome sequencing, we found the effect of internal systemic environment on epithelial cells after carbon black exposure was an inflammatory response, which mainly activates cell cycle-related pathways. After exposure to carbon black, the internal systemic environment could activate cancer-related pathways like epithelial-mesenchymal transition, hypoxia, TNF-α signaling via NF-κB. The hub genes in the carbon black group (CDC20 and PLK1) and their correlation with the systemic environment were uncovered by constructing the protein-protein interaction network. Inflammatory cytokines, especially CRP, were strongly correlated with the expression of CDC20 and PLK1. Besides, we also find a strong correlation between CDC20 and cytokinesis-block micronucleus endpoints in peripheral blood (rho = 0.591, P < 0.001). Our results show that long-term carbon black exposure might activate cell cycle-related pathways through circulating inflammation and increase the risk of cancer, while the oxidative stress caused by diesel exhaust particles are mainly related to PAHs exposure. After exposure to carbon black, the systemic environment could activate cancer-related pathways like diesel exhaust particles, increasing the risk of lung cancer. These attempts might provide a further understanding of the indirect effect of chronic occupational inhaled carbon black exposure on pulmonary carcinogenesis.

Artificial light at night (ALAN) is a major driver of firefly population declines, but its physiological effects are not well understood. To investigate the impact of ALAN on firefly development, we exposed larval Aquatica ficta fireflies to ALAN for two weeks. High larval mortality was observed in the periods of 1–68 days and 106–134 days post-treatment, which may represent the short- and long-term impacts of ALAN. We then profiled the transcriptome of larval Aquatica ficta fireflies following two weeks of ALAN exposure. A total of 1262 (1.67% out of 75777 unigenes) were differentially expressed in the treatment group: 1157 were down-regulated, and 105 were up-regulated. Up-regulated unigenes were related to regulation of hormone levels, ecdysteroid metabolic process, and response to stimulus; down-regulated unigenes were related to negative regulation of insulin receptor signaling, germ cell development, oogenesis, spermatid development, and regulation of neuron differentiation. Transcriptome results suggest that the endocrine, reproductive, and neural development of firefly larvae could be impaired by even relatively brief period of ALAN exposure. This report contributes a much-needed molecular perspective to the growing body of research documenting the fitness impacts of ALAN on bioluminescent fireflies.

Plastic particles, which are formed from routinely used plastics and their fragments, have become a new pollutant raising widespread concern about their potential effects. Several studies have been conducted to examine their toxicity, but the effects of nano-sized plastic fragments on freshwater organisms remain largely unclear and need to be further investigated. In this study, larval tilapia were first exposed to 100 nm polystyrene nanoparticles (PS-NPs, 20 mg/L) for seven days and then returned to freshwater without PS-NPs for another seven days in order to determine the toxic effects of PS-NPs at both transcriptomic and metabolomic levels. A total of 203 significantly changed metabolites, and 2,152 differentially expressed unigenes were identified between control and PS-NP treatment groups, control and recovery groups, as well as treatment and recovery groups. Our data suggested that PS-NPs induced abnormal metabolism of glycolipids, energy, and amino acids in tilapia after short-term exposure. Additionally, PS-NPs caused disturbed signaling, as suggested by the transcriptomic results. Different transcriptomic and metabolomic levels between the treatment group and recovery group indicated a persistent impact of PS-NPs on tilapia. The presence of adhesion molecule-related differentially expressed genes (DEGs) suggested that PS-NPs might cause early inflammatory responses. Notably, the detection of chemical stimulus involved in the sensory perception of smell was the most severely impacted biological process. Our work systemically studied the ecotoxicity of nano-sized plastics in aquatic creatures at the molecular and genetic levels, serving as a basis for future investigations on the prevention and treatment of such pollutants.

Identifying the adverse impacts of pesticide exposure is essential to guide regulations that are protective of wildlife and human health. Within rice ecosystems, amphibians are valuable indicators because pesticide applications coincide with sensitive reproductive and developmental life stages. We conducted two experiments using wild cane toads (Rhinella marina) to test 1) whether environmentally relevant exposure to a commercial formulation of butachlor, an acetanilide herbicide used extensively in rice, affects amphibian development and 2) whether cane toad tadpoles are capable of acclimatizing to sub-lethal exposure. First, we exposed wild cane toads to 0.002, 0.02, or 0.2 mg/L of butachlor (Machete EC), during distinct development stages (as eggs and hatchlings, as tadpoles, or continuously) for 12 days. Next, we exposed a subset of animals from the first experiment to a second, lethal concentration and examined survivorship. We found that cane toads exposed to butachlor developed slower and weighed less than controls, and that development of the thyroid gland was affected: exposed individuals had smaller thyroid glands and thyrocyte cells, and more individual follicles. Analyses of the transcriptome revealed that butachlor exposure resulted in downregulation of transcripts related to metabolic processes, anatomic structure development, immune system function, and response to stress. Last, we observed evidence of acclimatization, where animals exposed to butachlor early in life performed better than naïve animals during a second exposure. Our findings indicate that the commercial formulation of butachlor, Machete EC, causes thyroid endocrine disruption in vertebrates, and suggest that exposure in lowland irrigated rice fields presents a concern for wildlife and human health. Furthermore, we establish that developmental assays with cane toads can be used to screen for adverse effects of pesticides in rice fields.

Nitrate is a major pollutant component in ambient PM₂.₅. It is known that chronic exposure to PM₂.₅ NO₃⁻ damages respiratory functions. We aim to explore the underlying toxicological mechanism at single cell resolution.We systematically conducted exposure experiments on forty C57BL/6 mice, assessed respiratory functions, and profiled lung transcriptome. . Afterward, we estimated the cell type compositions from RNA-seq data using deconvolution analysis. The genes and pathways associated with respiratory function and dysregulated by to PM₂.₅ NO₃⁻ exposure were characterized at bulk-tissue and single-cell resolution.PM₂.₅ NO₃⁻ exposure did not significantly modify the cell type composition in lung, but profoundly altered the gene expression within each cell type. At ambient concentration (22 μg/m³), exposure significantly (FDR<10%) altered 95 genes’ expression. Among the genes associated with respiratory functions, a large fraction (74.6–91.7%) were significantly perturbed by PM₂.₅ NO₃⁻ exposure. For example, among the 764 genes associated with peak expiratory flow (PEF), 608 (79.6%) were affected by exposure (p = 1.92e-345). Pathways known to play role in lung disease pathogenesis, including circadian rhythms, sphingolipid metabolism, immune response and lysosome, were found significantly associated with respiratory functions and disrupted by PM₂.₅ NO₃⁻ exposure.This study extended our knowledge of PM₂.₅ NO₃⁻ exposure’s effect to the levels of lung gene expression, pathways, lung cell type composition and cell specific transcriptome. At single cell resolution, we provided insights in toxicological mechanism of PM₂.₅ NO₃⁻ exposure and subsequent pulmonary disease risks.