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Cadmium (Cd) and lead (Pb) are the primary hazardous heavy metals that accumulate in crops and pose substantial risks to public health via the food chain. Limiting the migration of these toxic metals from contaminated environments to rice is the most direct and crucial remediation approach. Bioremediation with microorganisms has been extensively utilized for managing heavy metal contamination in the natural environment, and the interplay between microbes and crops is important to alleviate heavy metal stress. Here, we express Lpp-OmpA fused with two metal-binding domains (PbBD and MTT5) in the outer membrane of Deinococcus radiodurans to enhance both Cd and Pb adsorption. Our results showed that the recombinant strain LOPM, which displayed an increased tolerance to both Cd and Pb stress, exhibited a 4.9-fold higher Cd adsorption and 3.2-fold higher Pb adsorption compared to wild-type strain R1. After LOPM cells colonized the rice root, Cd content reduced to 47.0% in root and 43.4% in shoot; Pb content reduced to 55.4% in root and 26.9% in shoot, as compared to the plant’s exposure to Cd and Pb. In addition, cells of LOPM strain colonized on rice roots alleviate Cd- and Pb-induced oxidative stress by reducing ROS levels and enhancing antioxidant enzyme activities in rice. This study supplies a promising application of genetic-engineering extremophile bacteria in reducing heavy metal accumulation and toxicity in rice.

Mutations in AT‐rich interactive domain‐containing protein 1A (ARID1A) cause Coffin‐Siris syndrome (CSS), a rare genetic disorder that results in mild to severe intellectual disabilities. However, the biological role of ARID1A in the brain remains unclear. In this study, we report that the haploinsufficiency of ARID1A in excitatory neurons causes cognitive impairment and defects in hippocampal synaptic transmission and dendritic morphology in mice. Similarly, human embryonic stem cell‐derived excitatory neurons with deleted ARID1A exhibit fewer dendritic branches and spines, and abnormal electrophysiological activity. Importantly, supplementation of acetate, an epigenetic metabolite, can ameliorate the morphological and electrophysiological deficits observed in mice with Arid1a haploinsufficiency, as well as in ARID1A ‐null human excitatory neurons. Mechanistically, transcriptomic and ChIP‐seq analyses demonstrate that acetate supplementation can increase the levels of H3K27 acetylation at the promoters of key regulatory genes associated with neural development and synaptic transmission. Collectively, these findings support the essential roles of ARID1A in the excitatory neurons and cognition and suggest that acetate supplementation could be a potential therapeutic intervention for CSS. Synopsis Mutations in ARID1A cause Coffin‐Siris syndrome (CSS), a rare genetic disorder with severe neurodevelopmental deficits. This study investigates the genetic basis of the pathophysiological role of ARID1A in CSS and proposes a potential therapeutic intervention. Arid1a haploinsufficiency in mouse excitatory neurons leads to spatial memory defects. ARID1A is required for neuron dendritic and synapse growth in mice and humans. Acetate supplementation rescues the neuronal deficits by increasing H3K27 acetylation levels at the promoters of neuronal genes in both Arid1a haploinsufficient mice and ARID1A KO hESC‐derived neurons. Graphical Abstract Mutations in ARID1A cause Coffin‐Siris syndrome (CSS), a rare genetic disorder with severe neurodevelopmental deficits. This study investigates the genetic basis of the pathophysiological role of ARID1A in CSS and proposes a potential therapeutic intervention.

Iron-binding proteins, known as ferritins, play pivotal roles in immunological response, detoxification, and iron storage. Despite their significance to organisms, little is known about how they affect the immunological system of the red swamp crayfish ( Procambarus clarkii ). In our previous research, one ferritin subunit was completely discovered as an H-like subunit ( PcFeH ) from P. clarkii . The full-length cDNA of PcFerH is 1779 bp, including a 5’-UTR (untranslated region, UTR) of 89 bp, 3’-UTR (untranslated region, UTR) of 1180 bp and an ORF (open reading frame, ORF) of 510 bp encoding a polypeptide of 169 amino acids that contains a signal peptide and a Ferritin domain. The deduced PcFerH protein sequence has highly identity with other crayfish. PcFerH protein’s estimated tertiary structure is quite comparable to animal structure. The PcFerH is close to Cherax quadricarinatus , according to phylogenetic analysis. All the organs examined showed widespread expression of PcFerH mRNA, with the ovary exhibiting the highest levels of expression. Additionally, in crayfish muscles, intestines, and gills, the mRNA transcript of PcFerH was noticeably up-regulated, after LPS and Poly I:C challenge. The expression of downstream genes in the immunological signaling system was suppressed when the PcFerH gene was knocked down. All of these findings suggested that PcFerH played a vital role in regulating the expression of downstream effectors in the immunological signaling pathway of crayfish.

is an extreme bacterium known for its high resistance to stresses including radiation and oxidants. The ability of to reduce Au(III) and biosynthesize gold nanoparticles (AuNPs) was investigated in aqueous solution by ultraviolet and visible (UV/Vis) absorption spectroscopy, electron microscopy, X-ray diffraction (XRD), dynamic light scattering (DLS), Fourier transform infrared spectroscopy (FTIR) and X-ray photoelectron spectroscopy (XPS). efficiently synthesized AuNPs from 1 mM Au(III) solution in 8 h. The AuNPs were of spherical, triangular and irregular shapes with an average size of 43.75 nm and a polydispersity index of 0.23 as measured by DLS. AuNPs were distributed in the cell envelope, across the cytosol and in the extracellular space. XRD analysis confirmed the crystallite nature of the AuNPs from the cell supernatant. Data from the FTIR and XPS showed that upon binding to proteins or compounds through interactions with carboxyl, amine, phospho and hydroxyl groups, Au(III) may be reduced to Au(I), and further reduced to Au(0) with the capping groups to stabilize the AuNPs. Biosynthesis of AuNPs was optimized with respect to the initial concentration of gold salt, bacterial growth period, solution pH and temperature. The purified AuNPs exhibited significant antibacterial activity against both Gram-negative ( ) and Gram-positive ( ) bacteria by damaging their cytoplasmic membrane. Therefore, the extreme bacterium can be used as a novel bacterial candidate for efficient biosynthesis of AuNPs, which exhibited potential in biomedical application as an antibacterial agent.

Background Nanoplastics have been recently found widely distributed in our natural environment where ubiquitously bacteria are major participants in various material cycles. Understanding how nanoplastics interact with bacterial cell membrane is critical to grasp their uptake processes as well as to analyze their associated risks in ecosystems and human microflora. However, little is known about the detailed interaction of differentially charged nanoplastics with bacteria. The present work experimentally and theoretically demonstrated that nanoplastics enter into bacteria depending on the surface charges and cell envelope structural features, and proved the shielding role of membrane lipids against nanoplastics. Results Positively charged polystyrene nanoplastics (PS-NH 2 , 80 nm) can efficiently translocate across cell membranes, while negatively charged PS (PS-COOH) and neutral PS show almost no or much less efficacy in translocation. Molecular dynamics simulations revealed that the PS-NH 2 displayed more favourable electrostatic interactions with bacterial membranes and was subjected to internalisation through membrane penetration. The positively charged nanoplastics destroy cell envelope of Gram-positive B. subtilis by forming membrane pore, while enter into the Gram-negative E. coli with a relatively intact envelope. The accumulated positively charged nanoplastics conveyed more cell stress by inducing a higher level of reactive oxygen species (ROS). However, the subsequently released membrane lipid-coated nanoplastics were nearly nontoxic to cells, and like wise, stealthy bacteria wrapped up with artifical lipid layers became less sensitive to the positively charged nanoplastics, thereby illustrating that the membrane lipid can shield the strong interaction between the positively charged nanoplastics and cells. Conclusions Our findings elucidated the molecular mechanism of nanoplastics’ interaction and accumulation within bacteria, and implied the shielding and internalization effect of membrane lipid on toxic nanoplastics could promote bacteria for potential plastic bioremediation. Graphical Abstract

Nanoplastics are emerging pollutants of global concern. Agricultural soil is becoming a primary sink for nanoplastics generated from plastic debris. The uptake and accumulation of nanoplastics by crops contaminate the food chain and pose unexpected risks to human health. However, whether nanoplastics can enter grains and their impact on the grains of crop grown in contaminated soil is still unknown. Here, the translocation of polystyrene nanoplastics (PS‐NPs) in crops, including peanut (Arachis hypogaea L.) and rice (Oryza sativa L.) is investigated. It is demonstrated PS‐NPs translocation from the root and accumulation in the grains at the maturation stage. The treatment with PS‐NPs (250 mg kg−1) increases the empty‐shell numbers of rice grain by 35.45%, thereby decreasing the seed‐setting rate of rice by 3.02%, and also decreases the average seed weight of peanuts by 3.45%. Moreover, PS‐NPs exerted adverse effects on nutritional quality, such as decreasing the content of mineral elements, amino acids, and unsaturated fatty acids. To the knowledge, this is the first report of the presence of nanoplastics in the grains of crop plants grown in soil containing nanoplastics, and the results highlight the impact of nanoplastics on the yield and nutritional quality of crop grains. This study demonstrates that polystyrene nanoplastics could accumulate in crop grains, and pose adverse effects on nutritional quality of crop grains. Considering the ubiquitous distribution of plastic debris, the uptake and accumulation of nanoplastics by crops can contaminate the food chain, pose negative impacts on the crop economy and also may bring unexpected risks to human health.

Objective Neurodevelopmental diseases are common disorders caused by the disruption of essential neurodevelopmental processes. Recent human exome sequencing and genome‐wide association studies have shown that mutations in the subunits of the SWI/SNF (BAF) complex are risk factors for neurodevelopmental diseases. Clinical studies have found that ARID1A (BAF250a) is the most frequently mutated SWI/SNF gene and its mutations lead to mental retardation and microcephaly. However, the function of ARID1A in brain development and its underlying mechanisms still remain elusive. Methods The present study used Cre/loxP system to generate an Arid1a conditional knockout mouse line. Cell proliferation, cell apoptosis and cell differentiation of NSPCs were studied by immunofluorescence staining. In addition, RNA‐seq and RT‐PCR were performed to dissect the molecular mechanisms of Arid1a underlying cortical neurogenesis. Finally, rescue experiments were conducted to evaluate the effects of Neurod1 or Fezf2 overexpression on the differentiation of NSPCs in vitro. Results Conditional knockout of Arid1a reduces cortical thickness in the developing cortex. Arid1a loss of function inhibits the proliferation of radial glial cells, and increases cell death during late cortical development, and leads to dysregulated expression of genes associated with proliferation and differentiation. Overexpression of Neurod1 or Fezf2 in Arid1a cKO NSPCs rescues their neural differentiation defect in vitro. Conclusions This study demonstrates for the first time that Arid1a plays an important role in regulating the proliferation and differentiation of NSPCs during cortical development, and proposes several gene candidates that are worth to understand the pathological mechanisms and to develop novel interventions of neurodevelopment disorders caused by Arid1a mutations. Although Arid1a mutations are closely related to mental retardation and microcephaly, the function of Arid1a in brain development and its underlying mechanisms still remain elusive. The present study demonstrates for the first time that Arid1a plays an important role in regulating the proliferation and differentiation of neural stem/progenitor cells during cortical development, and proposes several gene candidates that are worth to understand the pathological mechanisms and to develop novel interventions of neurodevelopment disorders caused by Arid1a mutations.

Integrins are a large group of cell-surface proteins that are classified as transmembrane proteins. Integrins are classified into different types based on sequence variations, leading to structural and functional diversity. They are broadly distributed in animals and have a wide range of biological functions such as cell-to-cell communication, intracellular cytoskeleton organization, cellular signaling, immune responses, etc. Integrins are among the most abundant cell surface proteins in insects, exhibiting their indispensability in insect physiology. Because of their critical biological involvement in physiological processes, they appear to be a novel target for designing effective pest control strategies. In the current literature review, we first discuss the discovery and expression responses of integrins against various types of pathogens. Secondly, we examine the specific biological roles of integrins in controlling microbial pathogens, such as phagocytosis, encapsulation, nodulation, immune signaling, and so on. Finally, we describe the possible uses of integrins to control agricultural insect pests.

Increasing evidence is showing that necroptosis has unique clinical significance in the occurrence and development of multiple diseases. Here, we systematically evaluate the role of necroptosis in clear cell renal cell carcinoma (ccRCC) and analyze its regulatory patterns. First, we evaluated the expression and enrichment of necroptotic factors in ccRCC using gene set enrichment analysis (GSEA) and survival analysis in the expression profile from The Cancer Genome Atlas (TCGA) to demonstrate the overall mutation of necroptotic pathway genes. Then, we used unsupervised clustering to divide the samples into two subtypes related to necroptosis with significant differences in overall survival (OS) and subsequently detected the differentially expressed genes (DEGs) between them. Based on this, we constructed the necroptosis scoring system (NSS), which also performed outstandingly in hierarchical data. Finally, we analyzed the association between NSS and clinical parameters, immune infiltration, and the efficacy of immunotherapy containing immune checkpoint inhibitors (ICIs), and we suggested potential therapeutic strategies. We screened 97 necroptosis-related genes and demonstrated that they were dysregulated in ccRCC. Using Cox analysis and least absolute shrinkage and selection operator (LASSO) regression, a prognostic prediction signature of seven genes was built. Receiver operating characteristic (ROC) curves and Kaplan-Meier (KM) analyses both showed that the model was accurate, and univariate/multivariate Cox analysis showed that as an independent prognostic factor, the higher the risk score, the poorer the survival outcome. Furthermore, the predicted scores based on the signature were observably associated with immune cell infiltration and the mutation of specific genes. In addition, the risk score could potentially predict patients' responsiveness to different chemotherapy regimens. Specifically, Nivolumab is more effective for patients with higher scores. The necroptosis-related signature we constructed can accurately predict the prognosis of ccRCC patients and further provide clues for targeted, individualized therapy.

Malignant tumor is a major killer that seriously endangers human health. At present, the methods of treating tumors include surgical resection, chemotherapy, radiotherapy and immunotherapy. However, the survival rate of patients is still very low due to the complicated mechanism of tumor occurrence and development and high recurrence rate. Individualized treatment will be the main direction of tumor treatment in the future. Because only by understanding the molecular mechanism of tumor development and differentially expressed genes can we carry out accurate treatment and improve the therapeutic effect. MicroRNA (miRNA) is a kind of small non coding RNA, which regulates gene expression at mRNA level and plays a key role in tumor regulation. Ferroptosis is a kind of programmed death caused by iron dependent lipid peroxidation, which is different from apoptosis, necrosis and other cell death modes. Now it has been found that ferroptosis plays an important role in the occurrence and development of tumors and drug resistance. More and more studies have found that miRNAs can regulate tumor development and drug resistance through ferroptosis. Therefore, in this review, the mechanism of ferroptosis is briefly outlined, and the relationship between miRNAs and ferroptosis in tumors is reviewed.