Search Results (2,874)

Neural crest cells give rise to the craniofacial skeleton and multiple pigment cell lineages, yet how duplicated developmental regulators partition their ancestral functions after teleost-specific whole-genome duplication remains unclear. Here, we employed CRISPR/Cas9 to generate alx4a and alx4b single and double mutants in Nile tilapia (Oreochromis niloticus). By integrating phenotype, skeleton, transcriptome, quantitative PCR, and AlphaFold-based structural modeling analyses, we revealed their functional divergence. Loss of alx4a caused a regionally restricted reduction in iridophore-derived reflectance and abnormal cranial morphology, whereas alx4b single mutants showed no obvious phenotype under the conditions examined. By contrast, double mutants exhibited an almost complete loss of iridophore-derived structural coloration and substantially more severe cranial defects, accompanied by reduced calcein labeling in the opercular region, consistent with altered cranial mineralization. Skin transcriptomic and quantitative PCR analyses revealed marked downregulation of pnp4a and tfec, which are associated with iridophore differentiation and coloration, whereas no significant expression differences were detected for the iridophore survival-related genes ltk and mpv17. AlphaFold2-assisted HDOCK protein–DNA modeling yielded more favorable docking metrics for Alx4a than for Alx4b with the pnp4a promoter, supporting a potential Alx4a–pnp4a promoter interaction that requires experimental validation. In contrast, no significant genotype-dependent differences were detected in the measured abundance of melanophores, xanthophores, or erythrophores, and no obvious difference in gross dorsal-fin spine formation was observed under the conditions examined. Together, these findings reveal unequal functional contributions of alx4a and alx4b, with alx4a acting as the dominant paralog in iridophore-associated structural coloration and both paralogs contributing unequally to cranial development, and support pnp4a as a candidate downstream gene associated with Alx4a activity. Full article

In contrast to foreign nucleic acids, some of our own endogenously synthesized nucleic acids may become immunologically active without being considered “foreign”. For example, abnormalities in chromatin organization, transcription termination, ribonucleic acid (RNA) splicing, and RNA editing, together with damage to mitochondrial integrity, may render normally functional deoxyribonucleic acid (DNA) and RNA persistently available and aberrantly structured ligands for innate immunity. Z-DNA-binding protein 1 (ZBP1), recently identified as an important component of this innate immune system, recognizes both left-handed DNA (Z-DNA) and left-handed RNA (Z-RNA) using its tandem Z-alpha (Zα) domains and couples recognition of these conformational states to receptor-interacting serine/threonine-protein kinase 1 (RIPK1)-, receptor-interacting serine/threonine-protein kinase 3 (RIPK3)-, and mixed-lineage kinase domain-like pseudokinase (MLKL)-dependent inflammatory and cell-death pathways. More recent studies have also shown that ZBP1 plays a role in recognizing damaged self-nucleic acids associated with tauopathies, Alzheimer’s disease (AD), traumatic brain injury (TBI), and amyloid-associated neuroinflammation. The nucleic-acid forms associated with these conditions include transposable-element activation, extended repeat-containing transcripts, RNA–RNA duplexes or RNA:DNA hybrids, oxidized mitochondrial DNA (mtDNA), and intercellularly transferred nucleic acids, all of which may exhibit substrate structures compatible with Z-form formation. Signaling by ZBP1 does not occur simply based upon nucleic-acid abundance; rather, signaling occurs after prolonged exposure to a nucleic acid when it persists in a structurally competent state, sufficient receptors are present to bind its exposed regions, the receptor proteoforms are competent to participate in signaling, receptor-interacting protein homotypic interaction motif (RHIM)-dependent assembly occurs, and the appropriate adaptor molecules are present. Furthermore, the identity of the cell type expressing ZBP1 determines whether the response produces RIPK3–MLKL-dependent neuronal injury, microglia-mediated inflammation, apoptosis, or mixed cell death. Finally, competition with adenosine deaminase acting on RNA 1 (ADAR1), melanoma differentiation-associated protein 5 (MDA5), double-stranded RNA-dependent protein kinase (PKR), the cyclic guanosine monophosphate–adenosine monophosphate synthase–stimulator of interferon genes (cGAS–STING) pathway, and other nucleic-acid-sensing proteins divides the available pool of endogenous nucleic acids among the outcomes of immune tolerance, type I interferon (IFN-I) signaling, translational inhibition, neuroinflammation, and necroptosis. Full article

The cohesin complex is a highly conserved, ring-shaped protein assembly that plays fundamental roles in chromosome biology. Originally identified as the molecular glue that holds sister chromatids together from DNA replication until cell division, cohesin has since been recognized as a pleiotropic regulator of genome organization, gene expression, DNA repair, and cell fate determination. In embryonic stem cells (ESCs), cohesin’s functions extend beyond canonical sister chromatid cohesion to include the maintenance of three-dimensional (3D) chromatin architecture through DNA loop extrusion, regulation of pluripotency-associated transcriptional programs, and facilitation of homologous recombination-mediated DNA repair during the prolonged S phase. Recent discoveries have revealed that meiosis-specific cohesin components, particularly the α-kleisin subunit REC8 and its interacting partner STAG3, are expressed and functionally active in mitotic ESC chromosomes, where they contribute to chromosomal organization and sister chromatid cohesion in concert with mitotic RAD21-containing cohesin. Furthermore, the interplay between cohesin and condensin complexes at shared genomic binding sites has emerged as a critical determinant of chromosome topology, with cohesin depletion leading to aberrant condensin accumulation and chromosome hypercompaction. Importantly, perturbations in cohesin function not only impair ESC self-renewal but also direct lineage-specific differentiation, linking cohesin to stem cell fate determination. Germline mutations in cohesin and its regulators underlie a spectrum of developmental disorders termed cohesinopathies, while somatic mutations are frequently observed in various cancers. This review provides a comprehensive overview of the diverse roles of cohesin in chromosome structure, cell cycle regulation, and stem cell biology, with particular emphasis on recent findings in ESCs that illuminate the complex interplay between mitotic and meiotic cohesin complexes. Full article

We review a theoretical and experimental programme with the aim of understanding two intimately related fundamental phenomena in biophysics: (i) the classical analogue of Fröhlich phonon condensation in macromolecules driven out of thermal equilibrium and (ii) the consequent activation of long-range resonant electrodynamic intermolecular forces. Both phenomena are underpinned by explicit Hamiltonian models. The first is derived by applying the time-dependent variational principle (TDVP) to the quantum Wu–Austin model, producing a fully classical Hamiltonian in action-angle variables whose nonlinear rate equations exhibit a nonequilibrium phase transition: the channelling of supplied energy into the lowest-frequency collective mode. The second is grounded in a classical electrodynamic Hamiltonian for two coupled oscillating dipoles whose normal-mode structure predicts long-range (∼$1/r^3$) resonant interactions, absent at thermal equilibrium but activated by out-of-equilibrium collective oscillations. We also discuss a complementary Hamiltonian approach that connects Fröhlich’s rate equations directly to Hamilton’s equations of motion, clarifying the role of bath-mediated nonlinear coupling and the conditions for strong condensation at room temperature. In addition, the TDVP is applied to a Davydov–Holstein–Fröhlich Hamiltonian describing electron–phonon motion along the backbone of a specific DNA sequence and its cognate restriction enzyme, EcoRI: the time-domain Fourier cross-spectrum of the resulting electron currents exhibits a sharp co-resonance peak for the canonical recognition sequence that disappears upon randomisation, providing a sequence-specific electrodynamic signature of DNA–protein recognition. Experimental evidence from THz near-field spectroscopy, fluorescence correlation spectroscopy, and direct observation of protein clustering is reviewed in relation to these theoretical predictions. The results establish a coherent physical picture suggesting that metabolic energy supply can play a role in driving macromolecules into coherently oscillating states that activate selective, distance-reaching electrodynamic forces capable of contributing to the organisation of biochemical reactions in living matter. Full article

Peritoneal dialysis (PD) is an effective renal replacement therapy; however, its long-term use is limited by the detrimental effects of glucose-based PD fluids on the peritoneal membrane, contributing to fibrosis and ultrafiltration failure. Previous studies have demonstrated that high-glucose exposure promotes oxidative DNA damage through upregulation of thioredoxin-interacting protein (TXNIP) expression, resulting in reduced thioredoxin (Trx) activity. This study investigated strategies to reduce oxidative stress in human peritoneal mesothelial cells exposed to high glucose concentrations. TXNIP expression, Trx activity, intracellular oxidative stress levels, and oxidative DNA damage were analyzed. High-glucose exposure caused a dose-dependent increase in TXNIP expression, a 5–15% reduction in Trx activity, and increased intracellular oxidative stress levels and oxidative DNA damage. Pre-treatment with the ROS scavenger N-acetylcysteine (NAC) reduced these effects. These findings demonstrate that glucose-induced TXNIP upregulation disrupts cellular redox homeostasis, resulting in increased intracellular oxidative stress and oxidative damage. Antioxidant compounds may therefore represent promising therapeutic strategies to protect the peritoneal membrane and improve long-term outcomes in PD. Full article

Background/Objectives: The identification of novel therapeutic targets is imperative to overcome the limitations of current anti-toxoplasmosis treatments. This study aims to investigate the potential of repurposing Pentamidine as an inhibitor against the HMG-Box domain-containing protein (TGARI_247020) in Toxoplasma gondii, a protein hypothesized to be essential for the parasite’s genomic stability. Methods: The study utilized a multi-layered in silico approach. First, the biological essentiality of the target gene was validated by analyzing CRISPR-Cas9-based phenomics data from the ToxoDB database. Second, the structural properties of the HMG-Box domain (ID: A0A139YAG1) were characterized using AlphaFold models. Finally, molecular docking simulations were conducted via the SwissDock server to evaluate the binding affinity and interaction dynamics between Pentamidine and the target protein. Results: Genomic analysis revealed a phenotype score of −1.2, confirming the indispensable role of the TGARI_247020 gene for parasite viability. Structural analysis identified a well-defined binding pocket within the HMG-Box domain. Molecular docking results demonstrated a high binding affinity for Pentamidine, yielding an optimal AC Score of −44.93, supported by a FullFitness value of −1134.13 kcal/mol. The interaction was primarily stabilized by a network of hydrogen bonds and favorable steric fits within the catalytic groove of the protein. Toxoplasmosis is widely classified as a neglected parasitic disease, posing persistent public health challenges and veterinary economic concerns globally. Traditional de novo drug discovery is often hindered by high costs and prolonged timelines, making drug repositioning (repurposing) a highly attractive and cost-effective strategy to identify novel therapeutics from established clinical agents over the past decade. Computer-Aided Drug Design (CADD), particularly Structure-Based Drug Design (SBDD), has provided a robust molecular framework to prioritize candidate drugs against essential parasitic targets. In apicomplexan parasites, high-mobility group box (HMGB) proteins, such as TgHMGB1a, serve as critical nuclear architectural factors that bind to distorted DNA structures and modulate genomic transcription, disrupting these essential DNA–protein interactions, representing a promising, yet under-explored, therapeutic target. The hypothesis for evaluating Pentamidine—an aromatic dicationic diamidine traditionally used in African trypanosomiasis—lies in its established ability to interact with nucleic acids and block critical molecular targets in other protozoa, providing a logical biochemical rationale for testing its potential as a structural inhibitor of the T. gondii HMG-box protein. Conclusions: Our findings provide preliminary in silico evidence that Pentamidine targets the HMG-Box protein, suggesting its potential for drug repurposing. However, due to established clinical limitations of Pentamidine (such as nephrotoxicity and poor blood–brain barrier permeability), further experimental in vitro and in vivo validation is strictly required to evaluate its therapeutic efficacy. Full article

Chemokines are best known for orchestrating leukocyte migration; however, accumulating evidence indicates that mammalian CXCL14 also functions as a direct antimicrobial effector of innate immunity. Nevertheless, the molecular basis underlying the bactericidal activity of fish chemokines remains largely unexplored. In this study, we identified and functionally characterized Ctenopharyngodon idella CXCL14 (CiCXCL14) as a broad-spectrum antimicrobial protein. CiCXCL14 is predominantly expressed in immune-related organs and is significantly upregulated upon Aeromonas hydrophila challenge, suggesting an active role in antibacterial defense. Recombinant CiCXCL14 exhibited potent, concentration-dependent bactericidal activity against E. coli, A. hydrophila, P. fluorescens, A. veronii, S. aureus, and S. agalactiae. Time-kill assays further demonstrated that CiCXCL14 exhibited rapid bactericidal activity, achieving near-complete killing of S. aureus within 40 min and E. coli within 160 min. Mechanistically, CiCXCL14 disrupts bacterial membrane integrity and interacts with purified bacterial genomic DNA, indicating that membrane damage and DNA interaction may both contribute to its bactericidal activity. Notably, CiCXCL14 retained substantial antibacterial activity after heat treatment, whereas its activity gradually decreased with increasing NaCl concentrations. In vivo, administration of recombinant CiCXCL14 improved survival rates in grass carp challenged with a lethal dose of A. hydrophila and reduced bacterial burdens in the liver, spleen, and trunk kidney. Collectively, these findings identify CiCXCL14 as a teleost chemokine with direct antibacterial activity and demonstrate that it contributes to antibacterial defense through membrane disruption and interaction with bacterial DNA. These findings provide a foundation for future studies investigating the potential application of CiCXCL14 in aquaculture disease control. Full article

Porcine epidemic diarrhea virus (PEDV) G2c variants have recently emerged, posing significant challenges to swine health management. As a major coronavirus affecting the swine industry, PEDV exhibits extensive genetic variability, which has greatly complicated disease control. Current vaccines provide suboptimal protection under field conditions. Therefore, the isolation of recently circulating strains and the establishment of a robust reverse genetics system are critical for advancing the study of emerging variants and facilitating rational vaccine development. In this study, a PEDV field strain designated PEDV-BJ-2023 was isolated from diarrheic piglets in Guizhou, China. Phylogenetic analysis based on the complete genome and spike gene classified PEDV-BJ-2023 within the emerging G2c lineage. To facilitate functional studies, a full-length infectious cDNA clone was constructed using transformation-associated recombination cloning in yeast. Furthermore, an enhanced green fluorescent protein reporter virus was generated via CRISPR/Cas9-assisted homologous recombination by inserting an EGFP-2A cassette upstream of the nucleocapsid gene. The recombinant viruses displayed virion morphology and plaque characteristics similar to those of the parental wild-type PEDV-BJ-2023 strain, although the parental virus exhibited faster replication during the early stage of infection in vitro. In 5-day-old piglets, all three viruses caused severe diarrhea, weight loss, and intestinal lesions; however, recombinant viruses exhibited slightly reduced viral shedding and pathogenicity, with rPEDV-EGFP being the most attenuated. Notably, rPEDV-EGFP maintained stable EGFP expression over eight serial passages. This study establishes a reverse genetics platform for an emerging G2c PEDV strain and provides a stable fluorescent reporter virus, offering valuable tools for visualizing viral infection and investigating virus–host interactions. Full article

Protein arginine methyltransferases (PRMTs) are key regulators of diverse cellular processes in eukaryotes, including transcriptional regulation, RNA processing, signal transduction and DNA repair. However, the biological functions of PRMTs in Verticillium dahliae remain largely unexplored. In this study, we identified a PRMT1 homolog in V. dahliae. Targeted deletion of VdPRMT1 resulted in severely impaired hyphal growth, sporulation, stress responses and pathogenicity. Subcellular localization analysis showed that VdPRMT1 is distributed in both the nucleus and cytoplasm of hyphae. Host-induced gene silencing (HIGS) of VdPRMT1 in cotton significantly reduced disease severity, supporting its important role in pathogenicity. Furthermore, VdLuc7, a U1 snRNP-associated protein containing multiple RG/RGG motifs, was identified as a putative interacting partner of VdPRMT1 through yeast two-hybrid (Y2H) screening, bimolecular fluorescence complementation (BiFC) and luciferase complementation imaging (LCI) assays. Together, our results demonstrate that VdPRMT1 is required for normal fungal development and full virulence in V. dahliae, and suggest that arginine methylation may contribute to pathogenicity through regulation of RNA processing-related pathways. These findings provide new insights into the molecular mechanisms underlying fungal virulence and identify VdPRMT1 as a potential target for disease control. Full article

Polyphosphate (polyP) is an evolutionarily conserved linear polymer of orthophosphate residues with diverse functions across organisms from bacteria to mammals. In addition to its roles in phosphate and energy storage, polyP has been implicated in thrombosis, inflammation, cancer, metabolism, cytoskeletal regulation, and neurodegenerative diseases. PolyP also acts as a molecular scaffold interacting with lysine-rich proteins and may contribute to protein folding and amyloid formation. However, biochemical heterogeneity, including variation in chain-length, subcellular localisation, and supramolecular organisation together with the absence of clearly defined mammalian biosynthetic pathways, has limited mechanistic understanding of polyP biology. Reliable detection and quantification remain challenging because current methods often suffer from limited specificity, chain length bias, insufficient quantitative robustness, and interference from other highly anionic biomolecules such as DNA or RNA. This review summarises current methodologies for polyP detection and characterisation. Emerging polyP-specific probes, including recombinant polyP-binding domains derived from polyphosphatases and conserved histidine α-helical domains may improve qualitative and quantitative analysis of polyP in complex biological systems. Improved analytical strategies will be essential to define the physiological roles of polyP and evaluate its potential as a biomarker and therapeutic target. Full article

Cancer metastasis is the leading cause of cancer-related mortality, accounting for more than 90% of cancer deaths worldwide. However, the epigenetic mechanisms governing the metastatic cascade remain incompletely understood. Epigenetic reprogramming, including reversible changes in histone modifications, DNA methylation, chromatin remodeling, and non-coding RNA (ncRNA)-mediated regulation, enables tumor cells to acquire invasive, migratory, stem-like, and immune-evasive characteristics. During epithelial-to-mesenchymal transition (EMT), key epigenetic regulators such as histone deacetylases (HDACs), the Polycomb repressive complex 2 (PRC2) subunit EZH2, lysine-specific demethylase 1 (LSD1/KDM1A), and bromodomain and extraterminal (BET) proteins repress epithelial gene expression while activating mesenchymal transcriptional programs, promoting invasion and dissemination. At distant sites, epigenetic plasticity facilitates metastatic colonization through mesenchymal-to-epithelial transition (MET) and adaptive chromatin remodeling. Because these changes are reversible, they represent attractive therapeutic targets. HDAC, EZH2, LSD1/KDM1A, BET, and DNA methyltransferase (DNMT) inhibitors have shown promise in preclinical models of metastasis, with several advancing through clinical trials. Long non-coding RNAs, particularly HOTAIR, function as epigenetic scaffolds that reinforce metastatic programs, while reciprocal interactions between tumor cells and the tumor microenvironment (TME) drive epigenetic adaptations that promote immune evasion and metastatic progression. In addition, circulating tumor DNA (ctDNA) methylation signatures are emerging as minimally invasive biomarkers for assessing metastatic risk and monitoring treatment. This review summarizes current insights into the epigenetic regulation of cancer metastasis, evaluates emerging epigenetic therapies, and highlights translational opportunities to advance precision anti-metastatic strategies and improve patient outcomes. Full article

Esophageal squamous cell carcinoma (ESCC) is a highly prevalent malignancy worldwide. Moreover, ESCC remains poorly characterized at the molecular level, which contributes to limited therapeutic options and an overall poor prognosis. In this context, HMGA family members, which are overexpressed in tumors but almost absent in healthy adult tissues, seem to represent promising therapeutic targets. These proteins act by binding to AT-hook DNA-binding motifs and may regulate the expression of several genes associated with tumor progression. Therefore, integrating in silico, translational, and in vitro approaches, we investigated the functional consequences of blocking HMGA2–DNA interaction in ESCC tumor progression by using netropsin, a site-specific ligand for AT-rich DNA regions. Our results demonstrate that netropsin treatment significantly reduced cell viability, migration, and cell cycle progression, thereby promoting apoptosis. Furthermore, netropsin treatment was capable of partially reverting Epithelial–Mesenchymal Transition (EMT) activation associated with HMGA2 expression, by downregulating EMT activators, such as Slug and Twist. Finally, the netropsin treatment sensitizes ESCC cells to chemotherapeutic treatment with 5-Fluorouracil. Taken together, our findings highlight that AT binding-specific blockade could be correlated with the inhibition of HMGA2 and may reveal a promising approach to better understand ESCC progression. Full article

Background/Objectives: Salmonella enterica (S. enterica) is a major poultry-associated foodborne pathogen and a persistent public health concern. The global rise in antimicrobial resistance has accelerated the search for alternative control strategies, including the use of bacteriophages. However, their successful application requires a comprehensive evaluation of their biological performance, genomic safety, and functional proteins. This study aimed to characterize Salmonella phage WP110 and assess its potential as a biocontrol agent in broiler-associated production systems. Methods: Phage WP110 was evaluated against 251 S. enterica isolates from broiler-related sources. Adsorption kinetics, one-step growth, environmental stability (temperature and pH), and effective multiplicity of infection (MOI) were determined using Salmonella Kentucky S1H28. Whole-genome sequencing (WGS) and bioinformatic analyses were performed for genome annotation, taxonomic classification, and safety evaluation. In addition, protein structural prediction of a putative endolysin (WP110-gp057) was conducted using AlphaFold2, followed by structural comparison and molecular docking with peptidoglycan. Biocontrol efficacy was evaluated in contaminated rice husk, chicken meat, and on non-food materials. Results: Phage WP110 demonstrated a broad lytic spectrum, lysing 248/251 S. enterica isolates (98.8%). It adsorbed rapidly (within 3–15 min) to host cells and exhibited a latent period of ~20 min with a burst size of 134 particles per infected cell. Phage WP110 remained stable at 4–45 °C and pH 5–11 but was inactivated at ≥75 °C and pH 2. Complete bacterial inactivation in broth assay was achieved at an MOI of 10⁴. Genomic analysis revealed a 110,216 bp linear dsDNA genome (39.74% GC) comprising 204 ORFs, 25 tRNAs, and long direct terminal repeats, with no detectable antibiotic resistance genes. Phylogenetic and intergenomic analyses classified phage WP110 as a novel species within the genus Epseptimavirus. Structural modeling of WP110-gp057 revealed conserved catalytic residues and high structural similarity to T5 endolysin, while docking analysis supported a structurally plausible interaction with peptidoglycan at the predicted active-site groove, consistent with its proposed role in host cell wall degradation. In application models, phage WP110 significantly reduced Salmonella contamination in rice husk (up to 4.3 log CFU/g), chicken meat (up to 1.7 log CFU/g), and on non-food material surfaces (0.7–1.5 log CFU reduction). Conclusions: Phage WP110 is a broad-host-range lytic phage with favorable infection kinetics, environmental robustness, and genomic safety. Its functionally supported endolysin and strong antibacterial efficacy across broiler-associated matrices highlight its potential as a biocontrol agent for Salmonella mitigation in poultry value chain. Full article

The Short Tandem Repeat 3D Structure Database (STR3SD) is a web-based database that provides a comprehensive resource for structural biology research of short tandem repeats (STRs) in cancers and neurodegenerative diseases. STR3SD contains three-dimensional (3D) structures of STRs surveyed from literature. The data are organized into three main categories, including 3D structures of nucleic acids only, nucleic acids–protein complexes, and nucleic acids–ligand complexes. Under these categories, each entry is annotated with repeat type, molecular type (DNA or RNA), sequence, PDB ID, structural component, ligand name, structural determination method, experimental conditions (temperature, pH, and ion), PubMed ID, and interactive 3D structure view. The database is built on direct literature investigation by human experts and serves as a crucial tool for studying structures and functions of STRs in cancers and neurodegenerative diseases, supporting research on structural polymorphisms and pathogenic mechanisms of STRs, and facilitating drug design targeting STRs for disease therapy. Full article

Bacteria in the human intestinal tract express more than 46 million genes, suggesting that interbacterial communication and communication with human cells are well-controlled and synchronized. Many papers have been published on quorum sensing (QS) and other forms of bacterial communication, e.g., nanotubes, nanovibrations, and electromagnetism. Autoinducers (AIs) such as AI-1 N-acyl homoserine lactones (AHLs), AI-2 boron-containing furanosyl borate diesters, AI-3 pyrazinone derivatives, a combination of AI-3/Epi (epinephrine)/NE (norepinephrine), auto-inducer peptides (AIPs), and SdiA (suppressor of division inhibition), along with their receptors, have been well-studied. However, little is known about the roles of quantum mechanics, quantum tunneling, and quantum entanglement in bacterial communication. Most proposals are hypothetical and remain conceptual frameworks supported by indirect evidence rather than validated experiments. The wave-like behavior of ions (quantum tunneling) may facilitate crossing potential energy barriers, such as cell membranes, in concert with protein channels. If this is indeed the case, ions in a quantum-tunneling state would, hypothetically, be able to pass through any part of the cell membrane and cell wall. This would, in theory, enhance biochemical reactions, interbacterial communication, and interactions with human cells. The long-range signaling ability of quanta could allow bacterial cells to maintain contact over long distances, modify their metabolic activities, and activate DNA repair systems. The wave-like behavior of subatomic particles and molecules may cause nanovibrations and generate electromagnetic fields. We argue that electrical signals generated within a biofilm by quanta may attract distant cells and enable cross-species communication. We propose a hypothetical “two-pillar” bacterial communication system, i.e., QS and quantum mechanics/tunneling/entanglement (QMTE), and discuss the advantages of combining both. Full article