Search Results (429)

RNA tailing, the non-templated addition of nucleotides to RNA 3′ ends, is a conserved post-transcriptional modification that plays a critical role in regulating RNA metabolism. In plants, this process is primarily mediated by nucleotidyltransferase proteins (NTPs). In this review, we analyze current knowledge of plant NTPs by integrating evidence from genetic, biochemical, and phylogenetic analyses of the gene-family across model plants and crops. We summarize the composition and evolutionary diversification of the plant NTP gene family, with emphasis on lineage-specific expansion and conservation patterns. Using Arabidopsis thaliana as a reference framework, we then describe the molecular roles of NTPs in the tailing of distinct RNA classes, emphasizing how tail type and length confer context-dependent regulatory outcomes including stabilization versus degradation and processing/maturation versus clearance. We further examine the determinants of substrate choice, focusing on RNA type, terminal structure, and subcellular localization. Finally, we discuss the biological functions of NTP-mediated RNA tailing in plants, linking RNA tailing to development, stress responses, antiviral immunity, and agronomic traits in crops. We conclude by outlining key mechanistic and physiological challenges that define future directions for understanding and harnessing NTP-mediated RNA regulation. Collectively, this review provides an integrated framework for understanding how RNA tailing by NTPs shapes plant RNA metabolism and biological fitness. Full article

Collagen is the primary protein in the extracellular matrix of human cells and the body and is essential for cell structure and function. Here, for the first time, we report a method for producing recombinant triple-helical collagen type III (rhCOL3) in transgenic tobacco as a bioreactor. We constructed a pMDV-COL3A1 vector containing the human type III collagen gene COL3A1, as well as a pMDV-COL3A1:5E vector that coexpressed COL3A1 and the enzymes required for its posttranslational modification. These two vectors were used to transform tobacco genetically. The COL3A1 gene was successfully coexpressed in tobacco plants with four enzymes that promote its posttranslational modification. The transcriptional level of COL3A1 in the transgenic lines coexpressing posttranslational modification genes was greater than that in the transgenic lines expressing only COL3A1. The enzyme-modified recombinant collagen was subsequently purified from a COL3A1:5E transgenic line. Our experimental results demonstrated that the terminal propeptides of plant-derived rhCOL3 can be correctly cleaved through the enzymatic hydrolysis of procollagen by coexpressed procollagen C proteinase (PCP) and procollagen N proteinase (PNP). The plant-derived rhCOL3 was thermally stable because the purified peptide chains can form a triple helix structure. Experiments have shown that plant-derived rhCOL3 has biological activity. In this study, functional recombinant full-length mature type III collagen with a triple-helix structure was successfully expressed in tobacco, providing a foundational plant-made material for future applications of collagen in human skin and bone repair in regenerative medicine. Full article

The efficacy of stigmasterol (STG) has not been previously evaluated in post-traumatic stress disorder (PTSD) models. Mice exposed to single prolonged stress with foot shock (SPS + FS) received oral STG (25 or 50 mg/kg) for 14 days. Serum corticosterone and serotonin levels were measured, anxiety and cognition were assessed, synaptic plasticity-related proteins and genes were quantified, and neuronal nitric oxide synthase (nNOS), nitric oxide (NO) accumulation, nNOS-postsynaptic density protein 95 (PSD95), and nNOS-carboxy-terminal PDZ ligand of nNOS (CAPON) interactions were evaluated. STG significantly reduced serum corticosterone levels and increased serotonin levels altered by SPS+FS exposure. Behavioral analyses revealed attenuation of anxiety-like behavior and cognitive deficits. STG increased hippocampal synaptic plasticity-related proteins and genes and increased the number and maturation of doublecortin⁺ cells. Additionally, STG suppressed the PTSD-induced nNOS overactivation and NO accumulation in the hippocampus and serum, and altered nNOS-PSD95 and nNOS-CAPON associations in the hippocampus. Together, these findings provide integrated in vivo evidence suggesting that STG may influence stress-related neurobiological pathways relevant to PTSD. Full article

Single-crystal diamond (SCD) demonstrates immense potential in high-power electronics, quantum information, and precision sensing due to its exceptional hardness, high thermal conductivity, wide bandgap, and superior chemical stability. Focusing on the crystallographic dependence of chemical vapor deposition (CVD) synthesis, this review systematically examines the growth mechanisms, defect characteristics, and application progress of typical low-index planes, specifically (100), (111), and (110). The (100) plane, leveraging stable step-flow growth modes and a mature process window, has established itself as the primary orientation for large-size, high-quality homoepitaxy. Conversely, while the (111) plane faces challenges regarding growth rate and the suppression of twins and stacking faults, it offers unique advantages for high-efficiency doping and the preferential alignment of quantum color centers, such as NV and SiV centers. The (110) plane, characterized by its anisotropic surface structure and high effective growth rate, shows significant potential for textured film preparation, N-type doping epitaxy, and quantum sensing based on surface termination control. Furthermore, this article outlines progress in high-index planes (e.g., (113)) and hexagonal diamonds (HDs), highlighting their possibilities for rapid thick-film deposition, directional color center regulation, and novel superhard/quantum material design. Finally, from an integrated “Material-Defect-Device” perspective, we identify current critical scientific and engineering challenges, providing a roadmap for the synergistic optimization of crystal plane selection, defect engineering, and device structure. Full article

The optimal timing of chemical defoliation is a critical bottleneck in stabilizing yield and fiber quality for short-season cotton, particularly under the intensifying pressure of mechanized global production. Current practices rely heavily on population-level boll opening rates, often overlooking the physiological maturity of late-season bolls. Here, we investigate the trade-offs between late-boll development and defoliation-induced senescence in short-season summer cotton. Our results demonstrate that defoliation timing based on a specific heat-unit or temporal threshold after flowering—rather than simple visual indicators—is essential for maximizing biological potential. We identified a critical physiological window (43 days post-anthesis) that synergistically optimizes boll weight, seed cotton yield, and fiber micronaire. Beyond this window, delayed defoliation leads to excessive fiber coarsening and reduced spinnability, while earlier application terminates dry matter accumulation prematurely, incurring significant yield penalties. These findings provide a mechanistic basis for synchronizing reproductive maturation with mechanical harvesting requirements. By establishing a precision defoliation framework, this study offers a scalable strategy to enhance the economic sustainability and resource-use efficiency of short-season cotton systems in double-cropping regions globally. Full article

Hydrogenated amorphous silicon (a-Si:H) is a mature thin-film technology for large-area devices and thin-film sensors, and its low-temperature growth via Plasma-Enhanced Chemical Vapor Deposition (PECVD) makes it particularly suitable for biomedical flexible and wearable platforms. However, the reliable integration of a-Si:H sensors on polymer substrates requires a quantitative assessment of their electrical stability under mechanical stress, since bending-induced variations may affect sensor accuracy. In this work, we provide a quantitative, direction-dependent evaluation of the static-bending robustness of both single-doped a-Si:H layers and complete p-i-n junction stacks on polyimide (Kapton^®), thereby linking material-level strain sensitivity to device-level functionality. First, n- and p-doped a-Si:H layers were deposited on 50 µm thick Kapton^® and then structured as two-terminal thin-film resistors to enable resistivity extraction under bending conditions. Electrical measurements were performed on multiple samples, with the current path oriented either parallel (longitudinal) or perpendicular (transverse) to the bending axis, and resistance profiles were determined as a function of bending radius. While n-type layers exhibited limited and mostly gradual variations, p-type layers showed a stronger sensitivity to mechanical stress, with a critical-radius behavior under transverse bending and a more progressive evolution in the longitudinal one. This directional response identifies a practical bending condition under which doped layers, particularly p-type films, are more susceptible to strain-induced degradation. Subsequently, a linear array of a-Si:H p-i-n sensors was fabricated on Kapton^® substrates with two different thicknesses (25 and 50 µm thick) and characterized under identical bending conditions. Despite the increased strain sensitivity observed in the single-layers, the p-i-n diodes preserved their rectifying behavior down to the smallest radius tested. Indeed, across the investigated radii, the reverse current at −0.5 V remained consistent, confirming stable junction operation under bending. Only minor differences, related to substrate thickness, were observed in the reverse current and in the high-injection regime. Overall, these results demonstrate the mechanical robustness of stacked a-Si:H junctions on polyimide and support their use as sensors for wearable biosensing architectures. By establishing a quantitative, orientation-aware stability benchmark under static bending, this study supports the design of reliable a-Si:H flexible sensor platforms for curved and wearable surfaces. Full article

The scorpion family Buthidae, renowned for its neurotoxin-rich venoms, dominates toxinology, while non-buthid venoms remain largely unexplored. Here, we present a comprehensive proteomic and biochemical characterization of the Amazonian chactid scorpion Brotheas amazonicus venom (BamazV), with emphasis on molecular complexity, proteolytic processing, and peptide diversity. Using an integrative venomics approach that combines molecular mass-based fractionation, reversed-phase chromatography, high-resolution mass spectrometry, N-terminal sequencing, and functional and immunological analyses, we reveal an unexpectedly complex venom profile enriched in high-molecular-weight components and extensively processed peptides, with more than 40 venom peptides sequenced by MS/MS and Edman degradation. The data provide evidence for non-canonical proteolytic events, including the generation of peptides from precursor regions not classically associated with mature venom components. In contrast to the venom of Tityus serrulatus, BamazV displays a “hydrolase-rich, neurotoxin-poor” profile, featuring a catalytically active Group III phospholipase A₂ (BamazPLA₂), a highly active hyaluronidase, metalloproteases, low-mass peptides, and potassium channel toxins. Our results suggest a hydrolytic prey-subjugation strategy, and limited cross-reactivity with commercial antivenom highlighted its distinct structural landscape. Overall, this study advances the understanding of venom evolution and proteolytic diversification in underexplored scorpion lineages, positioning B. amazonicus as a valuable model for investigating alternative venom strategies and identifying novel biotechnological scaffolds. Full article

In the face of mounting complexity in container terminal operations, the selection of an effective information system is paramount. The TOS (Terminal Operating System) is the most significant of all the information systems in existence for terminals. The objective of this study is to establish a set of criteria for selecting container TOS, determine the priority weights of these criteria and investigate their interactions. To the author’s knowledge, this is the first study to address this topic in such a detailed context. The hybrid FAHP (Fuzzy Analytic Hierarchy Process) and F-DEMATEL (Fuzzy Decision-Making Trial and Evaluation Laboratory) methodology was employed for the 18 criteria that were identified through the academic literature and expert views. The findings demonstrated that container terminal operators have expressed an expectation for a TOS structure that integrates complex business processes, provides effective decision support, increases traceability, works in harmony with advanced technologies, supports smart port transformation processes, enhances digital maturity and enables rapid intervention in bottlenecks. Furthermore, the fact that TOSs should support integration with external stakeholders is also critical in terms of collaboration and transparency, which are of great importance in supply chain management. It is hoped that the present study will contribute to the relevant literature and also provide a structural framework for terminal operators to select the most suitable TOS and for providers to design the most effective product. Full article

Runx2 plays essential roles in osteoblast differentiation and chondrocyte maturation. Runx2 in the perichondrium has been reported to inhibit chondrocyte maturation through Fgf18 induction. To further investigate the functions of Runx2 in the perichondrium, we generated Runx2^fl/−Cre mice by crossing Runx2^fl/+, Runx2^+/−, and 2.3-kb Col1a1 Cre mice and compared them with Runx2^fl/− mice at E15.5, when the endochondral bones were cartilaginous. Skeletal preparation of the upper limbs in Runx2^fl/−Cre mice showed reduced mineralization of the humerus and scapula, and histological analysis of the femurs showed delays in the terminal differentiation of chondrocytes, as indicated by the absence of mineralization and Spp1 expression in the cartilage and osteoblast differentiation in the perichondrium, compared to those in Runx2^fl/− mice. mRNA sequence analysis showed that the expression of Nell1, which encodes a secreted protein that enhances chondrocyte maturation, in Runx2^fl/−Cre femurs was more than two-fold lower than that in Runx2^fl/− femurs. Nell1 expression was reduced in the perichondrium of Runx2^fl/−Cre femurs compared to that in Runx2^fl/− femurs. Nell1 expression was upregulated by Runx2 overexpression and downregulated by Runx2 siRNA. These findings indicate that Runx2 in perichondrial osteoblasts enhances the terminal differentiation of chondrocytes by inducing Nell1 expression. Full article

Malaria remains a major global health burden, and the emergence of resistance to blood stage antimalarials underscores the need for new interventions targeting earlier stages of the parasite’s life cycle. The pre-erythrocytic liver stage represents a critical bottleneck and an attractive target for chemotherapeutic and prophylactic interventions. In this study, we functionally characterized the putative E3 ubiquitin ligase Trophozoite Exported Protein 1 (TEX1; PBANKA_0102200) in Plasmodium berghei using gene knockout, tagging, and imaging approaches across the mosquito and liver stages. TEX1 knockout parasites (PbTEX1-KO) showed impaired development during mosquito-stage transitions, with significant reductions in ookinete formation, oocyst numbers, and sporozoites reaching the salivary glands. In hepatic stages, TEX1-KO parasites displayed reduced growth, abnormal nuclear division, and impaired liver stage maturation, ultimately leading to a dramatic decline in detached cell formation and blood stage infectivity. Endogenous C-terminal tagging of TEX1 with GFP and 3×HA revealed a discrete subnuclear localization pattern, indicating a critical role in DNA synthesis and/or mitotic regulation. Our findings reveal that TEX1 is required for nuclear replication and division and successful development in both the mosquito and liver stages of Plasmodium. Given its pivotal role and nuclear localization during hepatic schizogony, TEX1 represents a promising target for the development of liver stage antimalarial interventions. Full article

Neuropeptide FF (NPFF) belongs to the RF-amide peptide family and is homologous to gonadotropin-inhibitory hormone (GnIH). The NPFF precursor encodes two mature peptides, NPFF and NPAF (neuropeptide AF). Both peptides share the conserved C-terminal PQRFa motif. However, there is very limited information available on receptor cross-reactivity for NPFF and GnIH peptides in teleosts. As a first step, we cloned two cognate receptor genes for NPFF, designated as NPFFR2-1 and NPFFR2-2, in the flatfish species half-smooth tongue sole. Tissue distribution analysis revealed that npffr2-1 and npffr2-2 transcripts were present at high levels in the brain and pituitary gland, and at lower levels in some peripheral tissues. In vitro functional analysis indicated that NPFF significantly stimulated CRE-luc and SRE-luc activity in COS-7 cells expressing either NPFFR2-1 or NPFFR2-2. However, NPAF increased CRE-luc and SRE-luc activity only via NPFFR2-1. Moreover, NPFF exerted an inhibitory effect on NFAT-RE-luc activity in COS-7 cells transfected with NPFFR2-1, whereas NPAF elicited an evident stimulatory effect via NPFFR2-2. Neither GnIH1 nor GnIH2 altered CRE-luc activity in COS-7 cells transfected with NPFFR2-1 or NPFFR2-2; however, forskolin-induced CRE-luc activity was significantly reduced by these two peptides. Furthermore, neither basal nor forskolin-stimulated CRE-luc activity was modified by NPFF or NPAF in COS-7 cells expressing the GnIH receptor (GnIHR). Both GnIH1 and GnIH2 significantly increased SRE-luc activity in COS-7 cells expressing NPFFR2-1 or NPFFR2-2, and vice versa. Taken together, our findings provide novel evidence that both NPFF and GnIH peptides could exert their functions via three different receptors, and that PKA, PKC, and Ca²⁺ signaling pathways are potential mediators. Full article

Background/Objectives: Mature adipocytes were previously regarded as terminally differentiated cells that are restricted to lipid storage. Recent studies have shown that they can dedifferentiate into fibroblast-like progenitor cells, termed dedifferentiated fat (DFAT) cells. These cells exhibit stem cell-like properties and multilineage potential, highlighting their promising role in regenerative medicine and disease pathology. This systematic review aims to explore and consolidate the evidence regarding mechanisms, culture methods, pathophysiological roles, and therapeutic potential of adipocyte dedifferentiation. Methods: A systematic review was conducted in PubMed using the terms “dedifferentiation”, “de-differentiation”, “transdifferentiation”, and related variants in combination with “adipocyte”. Studies were screened and selected according to the PRISMA 2020 guidelines. Non-English articles, non-full texts, and non-review papers were excluded. After duplicate removal and eligibility assessment, 53 studies were included. Further, these were classified into categories according to their abstracts. Results: The evidence from the included articles indicates that mature adipocytes can dedifferentiate both in vitro, via ceiling culture, and in vivo, yielding DFAT cells with proliferative and multilineage differentiation capacity. Dedifferentiation involves lipid droplet secretion (liposecretion) and is characterized by downregulation of adipogenic genes such as PPARG and C/EBPα, alongside upregulation of proliferation, stemness, and lineage-associated markers. Functionally, DFAT cells contribute positively to tissue regeneration and wound repair, but they can drive adverse outcomes such as fibrosis, insulin resistance, and tumor progression through signaling pathways, including Wnt/β-catenin and TGF-β. Conclusions: Mature adipocyte dedifferentiation marks a dynamic reprogramming mechanism with dual roles—beneficial in regenerative medicine and wound healing, yet detrimental in cancer and metabolic disease. Further research is required to identify in vivo regulators, establish definitive markers, and translate adipocyte plasticity into regenerative medicine applications. Full article

Ring Box Protein-1 (RBX1) is an essential component of the Skp1-cullin-F-box protein (SCF) E3 ubiquitin ligase, which is involved in the regulation of oocyte maturation in the form of ubiquitination substrate modification. In this study, a sequence of RBX1 (Sp-RBX1) was identified and analyzed using bioinformatics methods from the transcriptome data of Scylla paramamosain. The length of Sp-RBX1 cDNA sequence was 1247 bp, consisting of a 336 bp open reading frame (ORF). Sequence analysis revealed that the protein contained a C-terminal modified RING-H2 finger domain, with two zinc binding sites and a Cullin binding site, classifying it as a member of the RBX1 superfamily. The results of real-time fluorescence quantitative PCR (RT-qPCR) showed that Sp-RBX1 expression in the ovary was low at stages I and II, then significantly increased from stage III to V (p < 0.05), which indicated that it might be closely related to the maturation of oocytes. It also peaked at stage II in the hepatopancreas, then sharply declined from stages III to V. The expression pattern might be related to the accumulation of fat in the early development of hepatopancreas. Furthermore, we characterized the expression of Sp-RBX1 induced by follicle-stimulating hormone (FSH) and estradiol (E2) hormones. The results showed that the expression in the ovary was up-regulated by FSH and significantly inhibited by E2. The expression in the hepatopancreas increased only at 0.5 µmol/L concentration of FSH, and decreased in other groups. Conversely, it was up-regulated by E2. Thus, the expression of Sp-RBX1 was influenced by FSH in a concentration-dependent manner. These findings could offer valuable insights for further research on ovarian maturation in crustaceans. Full article

Transdifferentiation, also known as direct reprogramming, is the transformation of one terminally differentiated cell type into another mature cell type, while bypassing the stage of pluripotency. In leukemia, this phenomenon has a dual significance: on the one hand, it is an adaptive mechanism driving tumor survival and resistance to treatment, and on the other, it offers a potential opportunity for innovative therapies. Of particular interest is the directional transdifferentiation (mostly partial) toward dendritic cell-like phenotypes, which increases the immunogenicity of cancer cells. Mastering this process could define a new generation of immunotherapies that leverage the inherent plasticity of leukemic cells to achieve therapeutic benefits. In this brief review, we attempt to gather information concerning the molecular mechanism of this process and point to the role of dendritic cells as a crucial element of anticancer, particularly anti-leukemia innate and acquired, immunity. Thus, in vitro and in vivo techniques of inducing transformation of the leukemia cells into cancer antigen-presenting cells and the application of these technologies in current and future therapies are discussed. Full article

Alzheimer’s disease (AD) is neuropathologically characterized by tau-immunopositive neurofibrillary tangles (NFTs) and amyloid-β (Aβ)-immunopositive senile plaques. According to the widely accepted amyloid cascade hypothesis, Aβ pathology represents the upstream event in AD pathophysiology and induces tau aggregation. However, numerous studies have suggested that tau aggregates correlate more closely with neuronal loss and regional brain atrophy than with Aβ depositions. Tau aggregation in AD demonstrates a hierarchical spreading pattern beginning in the transentorhinal cortex, but the mechanisms underlying this spreading manner of lesions remain to be elucidated. This review aims to address current controversies regarding tau pathology in AD from the perspectives of both the ‘amyloid cascade’ and ‘tauopathy’ hypotheses. From the ‘amyloid cascade’ viewpoint, Aβ deposition prominently involves distal axon and axon terminals, and in some regions, there are anatomical correspondences between axonal Aβ pathology and cytoplasmic tau aggregations (e.g., a close relationship between senile plaques in the molecular layer of the hippocampal dentate gyrus and NFTs in the transentorhinal cortex). Nevertheless, this model cannot explain the whole body of hierarchical spreading of tau aggregation because notable spaciotemporal discrepancies also exist in many regions. From the ‘tauopathy’ perspective, the distribution of tau aggregates in AD involves key nodes within the memory circuits. Also, experimental studies have suggested that patient-derived tau exhibits seeding and neuron-to-neuron propagation properties. Interestingly, tau aggregation in AD appears to spread laterally in a proximity-dependent, cortico-cortical fashion rather than along long-range memory circuits. This contrasts with the system-selective, poly-nodal degenerations seen in four-repeat tauopathies, amyotrophic lateral sclerosis, or spinocerebellar degenerations. Moreover, the proportions of three-repeat and four-repeat isoforms shift during the maturation of NFTs in AD. Overall, spreading patterns of tau-pathology in AD cannot be fully explained by Aβ pathology and also differ from the system degeneration seen in other tauopathies. Full article