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Suzuki, M.

Publications and source records attributed to Suzuki, M..

At least 55 records · Page 3Linked to original sources

Specificity and mechanism of the double-stranded RNA-specific J2 monoclonal antibody

Double-stranded (ds) RNAs are major structural components of the transcriptome, hallmarks of viral infection, and primary triggers of innate immune responses. The J2 monoclonal antibody is the gold-standard method to discover and map endogenous dsRNAs across subcellular locations and cell surfaces, detect exogenous RNAs in viral infection, and surveil mRNA prophylactics and therapeutics for inflammatory dsRNAs. To define its epitope, specificity, and mechanism, we determine a 2.85 [A] co-crystal structure of J2 antigen-binding fragment (Fab) bound to dsRNA. J2 uses its heavy and light chains in tandem to track the dsRNA minor groove, recognizing a staggered 8-bp duplex. J2 is exquisitely selective for dsRNAs, requires 14 bp for robust binding, and exhibits greatly diminished binding for GC-rich dsRNAs. J2 and R-loop-specific S9.6 antibody share a common recognition strategy distinct from intracellular dsRNA-binding proteins. This study provides mechanistic insights into dsRNA recognition and establishes a framework for reliable application and data interpretation of the J2 antibody in RNA discovery.

molecular biology↗

β-III tubulin identifies anti-fibrotic state of pericytes in pulmonary fibrosis

Pericytes have been implicated in pulmonary fibrosis, yet their activated cellular states and functional roles remain largely unclear. Here, we identified {beta}-III tubulin (Tuj1) as a distinctive marker for fibrosis-associated lung pericytes. Most pericytes in fibrotic regions are Tuj1-positive and interact uniquely with multiple endothelial cells, localizing near collagen-producing fibroblasts and pro-fibrotic SPP1+/arginase+ macrophages. Tuj1 expression is predominantly induced in pericytes during the fibrotic phase, and Tuj1 gene (Tubb3) knockout in mice exacerbates lung fibrosis, accompanied by an increase in the neighboring pro-fibrotic fibroblasts and macrophages, suggesting an anti-fibrotic role for Tuj1-expressing pericytes. Mechanistically, the anti-fibrotic chemokine CXCL10 is upregulated in Tuj1-expressing pericytes, whereas this upregulation is not observed in Tubb3 knockout. Moreover, CXCL10 inhibits the pro-fibrotic differentiation of macrophages induced by lung fibroblasts in culture, implying that CXCL10 may mediate the anti-fibrotic effects of Tuj1-expressing pericytes. These findings underscore the role of lung pericytes in negatively regulating fibrotic process and their potential as therapeutic targets for pulmonary fibrosis patients. SummaryIn response to fibrotic stimuli, lung pericytes upregulate {beta}-III tubulin (Tuj1) expression, adopting an anti-fibrotic phenotype. This phenotype acts as a negative immune regulator of pro-fibrotic macrophage differentiation by releasing CXCL10, thereby counteracting the progression of pulmonary fibrosis.

pathology↗

Boosting Antitumour Efficacy and Immunity by Boron Neutron Capture Therapy with Size-Controlled Nanoparticles

Boron neutron capture therapy (BNCT) is emerging cancer radiotherapy requiring 10B sensitizer. Although boronophenylalanine (BPA)-BNCT is approved clinically in Japan, the low tumour selectivity and retentivity result in the long-time infusion of high doses. Based on our finding of the size-controllable mechanochemical synthesis of boron-10 carbide nanoparticles (10B4C NPs), the 50 nm size NPs grafted with poly(glycerol), {superscript 1}BC(50)-PG, is found to show superior tumour selectivity and retentivity to enhance the eradication efficacy at much lower dosage (5 mg [10B] / kg (mouse)). The dosage is further reduced by twice neutron irradiation or combination with an immune checkpoint inhibitor (ICI). Antitumour immunity is found to be boosted by {superscript 1}BC(50)-PG-BNCT to induce abscopal effect to treat remote or metastatic tumours and long-term memory to prevent cancer recurrence. Additionally, minimal side effects and gradual NP excretion are observed for one year. The 10B4C(50)-PG is concluded to be a promising 10B carrier for clinical application of BNCT due to the prominent antitumour efficacy and immune-activation with minimal toxicity.

cancer biology↗

Low-salinity medium for large-scale biomass production of the marine purple photosynthetic bacterium Rhodovulum sulfidophilum

Marine purple non-sulfur bacteria such as Rhodovulum sulfidophilum are versatile due to their diverse applications in bioremediation, biotechnological production of useful materials, industrial production of value-added compounds, and agricultural fertilizers. Our previous study demonstrated the potential of its lysed and dried biomass as a nitrogen fertilizer for plant production. However, large-scale fertilizer production requires scaling up the culture to larger volumes, which is not cost-effective with currently available options for growth media. In this study, we tested a seawater-based, cost-effective alternative to the commonly used nutrient-rich culture medium for the growth of this bacterium. We found that reducing salinity from 3% to 1.2% had no adverse effects on its heterotrophic growth, dry cell yield, nitrogen content, and total amino acid composition. The nitrogen content and the weight percent of free lysine, aspartic acid, and glutamate increased in the biomass obtained from cultures grown at 1.2% salinity. Under autotrophic conditions, decreasing salinity to 1.2% did not affect cell growth, final dry cell yields, and total carbon assimilation, but N assimilation tended to be higher. Reducing salinity to 1.2% proved to be cost-effective and feasible for the cultivation of R. sulfidophilum without increasing the risk of contamination, providing a viable alternative for its large-scale cultivation and application as a plant nitrogen fertilizer.

microbiology↗

Behavioral Manipulation of Ixodes scapularis by Ehrlichia muris eauclairensis: Implications for Tick-Borne Disease Transmission

Tick-borne diseases pose significant risks to both animals and humans, with emerging pathogens like Ehrlichia muris eauclairensis (EME) underscoring the need for a deeper understanding of pathogen-vector interactions and tick fitness. This study investigates the impact of EME on Ixodes scapularis nymphs, revealing significant behavioral changes in EME-positive ticks. These ticks exhibited increased movement speed, faster bite site-seeking for attachment, and prolonged feeding durations compared to control ticks. Proteomic analyses of the tick synganglion during resting and feeding phases identified 196 differentially expressed proteins in EME-positive ticks, including multiple proteins associated with nicotinic acetylcholine signaling pathways. Our findings indicated altered neuropeptide expression related to stimulus response and activity, suggesting changes in neurophysiology. This research provides the first evidence of behavioral manipulation by an Ehrlichia species, indicating that the tick nervous system is a site of bacterial influence and a potential target for interventions. These findings offer new insights into pathogen-vector dynamics that could lead to the development of transmission-blocking therapies, significantly impacting tick fitness and disease transmission. IMPORTANCETick-borne diseases (TBDs) are increasingly affecting humans, pets, and livestock, with cases rising in recent years. Ticks can carry multiple harmful germs, and human activities and environmental are contributing to new TBDs. This study shows that the bacteria Ehrlichia muris eauclairensis (EME) can change the behavior of nymphal black-legged ticks, which spread various diseases. Infected ticks moved faster, attached to hosts more quickly, and fed longer than uninfected ticks. These changes were linked to specific proteins in the ticks nervous system, suggesting that EME manipulates tick behavior. This is the first evidence that an Ehrlichia species can influence tick behavior, potentially increasing disease transmission. Understanding these interactions can help develop strategies to prevent TBDs by targeting the bacterias influence on ticks, ultimately reducing disease spread and improving public health.

microbiology↗

Pain-stimulated ultrasound vocalizations and their impact on pain response in mice

Pain is a complex phenomenon encompassing both the physiological and psychological aspects of sensation and emotion, respectively. In recent years, pain has been clarified to arise even without direct injury, with emotional transmission as a cause. However, the specific mechanisms behind emotional transmission are still not well understood. In this study, sounds in the ultrasonic domain that were recorded during pain stimulation in mice were used as sound stress to examine the effects of psychological stress caused by exposure to ultrasound on tactile thresholds. We also examined the effects of psychological stress caused by the ultrasound on an inflammatory pain model of mice. The tactile threshold decreased the next and three days after sound stress exposure in mice. DNA microarray analysis of the mouse thalamus exposed to sound stress revealed increased expression of inflammation-related genes, Prostaglandin-endoperoxide synthase 2 and C-X-C motif chemokine ligand 1. Their respective inhibitors, loxoprofen and SB225002, significantly improved hyperalgesia induced by sound stress. When sound stress was applied to a mouse model of inflammatory pain in which pain thresholds were restored 14 days after complete Freunds adjuvant administration, prolonged pain and attenuated analgesic effects of loxoprofen were observed. These results suggest that sound stress not only induces inflammation in the brain that causes hyperalgesia but may also be partially responsible for exacerbating inflammatory pain, hence complicating treatment.

pharmacology and toxicology↗

High-Resolution Proteomics Unveils Salivary Gland Disruption and Saliva-Hemolymph Protein Exchange in Plasmodium-Infected Mosquitoes

Plasmodium sporozoites, the stage that initiates a malaria infection, must invade the mosquito salivary glands (SGs) before transmitting to a vertebrate host. However, the effects of sporozoite invasion on salivary gland physiology and saliva composition remain largely unexplored. We examined the impact of Plasmodium infection on Anopheles gambiae salivary glands using high-resolution proteomics, gene expression, and morphological analysis. The data revealed differential expression of various proteins, including the enrichment of humoral proteins in infected salivary glands originating from the hemolymph. These proteins diffused into the SGs due to structural damage caused by the sporozoites during invasion. Conversely, saliva proteins diffused out into the circulation of infected mosquitoes. Moreover, infection altered saliva protein composition, as shown by proteomes from saliva collected from mosquitoes infected by P. berghei or P. falciparum, revealing a significant reduction of immune proteins compared to uninfected mosquitoes. This reduction is likely due to the association of these proteins with the surface of sporozoites within the mosquito salivary secretory cavities. The saliva protein profiles from mosquitoes infected with both Plasmodium species were remarkably similar, suggesting a conserved interaction between sporozoites and salivary glands. Our results provide a foundation for understanding the molecular interactions between Plasmodium sporozoites and mosquito salivary glands.

microbiology↗

A computational architecture incorporating shallow brain networks: integrating parallel cortical and subcortical processing

Artificial neural networks commonly have deep hierarchical structures that were originally inspired by the neuroanatomical evidence of cortico-cortical connectivity pattern found in the mammalian brain. Largely neglected in those models are non-hierarchical aspects of brain architecture, namely the subcortical pathways and the interactions between cortical and subcortical areas regardless of their hierarchical locations. Inspired by this principle, we present a computational model combining cortical hierarchical processing with subcortical pathways based on neuroanatomical evidence. We show the versatility of our model by implementing the cortical hierarchy in two alternative ways--a convolutional feedforward network and a predictive coding network. Both model variants can replicate behavioral observations in humans and monkeys on a perceptual context-dependent decision-making task. The model also reveals that subcortical structures lead decisions for easy trials while the more complex hierarchical network is necessary for the harder trials. Our results suggest that the parallel cortico-subcortical processing explored in the model represents a fundamental property that cannot be neglected in understanding the computational principles used by the brain. SignificanceArtificial intelligence and computational neuroscience models, particularly deep learning and predictive coding architectures, have been traditionally dominated by cortico-centric hierarchical frameworks. However, extensive neurobiological evidence suggests that cortical areas, regardless of their hierarchical classification, are deeply interconnected with subcortical structures in real brains. We propose here a computational framework demonstrating that parallel cortical-subcortical architectures can yield complex and more flexible computational capabilities, aligning with the observed behavior in the mammalian brain. Our model addresses key limitations in existing deep learning and predictive coding networks, offering a more biologically plausible and functionally advantageous alternative.

neuroscience↗

KEAP1 retention in phase-separated p62 bodies drives liver damage in autophagy-deficient conditions

Phase-separated p62 bodies activate NRF2, a key transcription factor for antioxidant response, by sequestering KEAP1, which targets NRF2 for degradation. Although p62 bodies containing KEAP1 are degraded by autophagy, they accumulate in various liver disorders. Their precise disease role remains unclear. We show that excessive KEAP1 retention in p62 bodies and NRF2 activation are major causes of liver damage when autophagy is impaired. In mice with weakened or blocked p62-KEAP1 interactions, KEAP1 retention and NRF2 activation under autophagy-deficient conditions were suppressed. Transcriptome and proteome analyses revealed that NRF2 targets upregulated by autophagy suppression normalized in p62 mutants unable to bind KEAP1. Autophagy deficiency caused organelle accumulation, especially of the ER, regardless of p62 mutation. Liver damage and hepatomegaly from autophagy suppression markedly improved in p62 mutants, particularly those with blocked KEAP1 binding. These findings highlight excessive KEAP1 retention in p62 bodies and defective organelle turnover as key drivers of liver pathology, underscoring the significance of phase separation in vivo.

cell biology↗

Spatiotemporal temperature control by holographic heating microscopy unveils cellular thermosensitive calcium signaling

Optical microheating technologies have revealed how biological systems sense heating and cooling at the microscopic scale. Sensing is based on thermosensitive biochemical reactions that frequently engage membrane proteins, Ca2+ channels, and pumps to convert sensing information as the Ca2+ signaling in cells. These findings highlight the feasibility of thermally manipulating intracellular Ca2+ signaling. However, how the thermosensitive Ca2+ signaling would behave, particularly in multicellular systems, remains elusive. In this study, to extend the ability of the spatiotemporal temperature control by optical microheating technologies, we propose holographic heating microscopy. Water-absorbable infrared (IR) laser light is modulated by a reflective liquid crystal on a silicon spatial light modulator (LCOS-SLM). A computer-generated hologram displayed on the LCOS-SLM modulates the spatial phase pattern of the IR laser light to generate predesigned temperature gradients at the microscope focal plane. The holographic heating microscopy visualizes how thermosensitive Ca2+ signaling is generated and propagated in MDCK cells, rat hippocampal neurons, and rat neonatal cardiomyocytes. Moreover, the optical control of the temporal temperature gradient reveals the cooling-rate dependency of Ca2+ signaling in HeLa cells. These findings demonstrate the extended ability of holographic heating microscopy in investigating cellular thermosensitivities and thermally manipulating cellular functions.

biophysics↗

Refined CRISPR/Cas9 genome editing in pea aphids uncovers the essential roles of Laccase2 in overwintering egg adaptation

The production of overwintering eggs is a critical adaptation for winter survival among many insects. Melanization contributes to eggshell pigmentation and hardening, consequently enhancing resistance to environmental stress. The complex life cycle of the pea aphid (Acyrthosiphon pisum), a model hemipteran insect with remarkable reproductive capacity, involves cyclical parthenogenesis. It enables the production of black overwintering eggs that undergo obligate diapause to survive under unfavorable conditions. Laccase2 (Lac2) is essential for cuticle sclerotization and pigmentation in other insects. We hypothesized that Lac2 plays a critical role in aphid eggshell pigmentation and survival during diapause. To test the hypothesis, we used CRISPR/Cas9 ribonucleoprotein microinjections and a novel Direct Parental CRISPR (DIPA-CRISPR) method to knockout Lac2. In Lac2 knockout (KO) crispants (G0), pigment-less eggs correlated with induced indel rates. Additionally, eggshell pigmentation was completely lost in homozygous Lac2 knockouts, leading to embryonic lethality. Observation of late-stage embryos in KO diapause eggs suggested that lethality occurred during late embryogenesis or hatching. Furthermore, eggshell stiffness was significantly reduced in Lac2 KOs, highlighting the role of this gene in eggshell hardening. Moreover, fungal growth was observed in KO eggs. These findings reveal the essential roles of Lac2 in eggshell pigmentation, hardening, late embryonic development, hatching, and fungal protection, which are critical for pea aphid survival during overwintering diapause. This study also advances CRISPR/Cas9-mediated genome editing in pea aphids by addressing the challenges associated with their unique biology, including complex life cycles, obligatory diapause, bacterial endosymbiosis, inbreeding depression, and high nuclease activity. Our optimized protocol achieved efficient targeted mutagenesis and germline transmission, thereby generating stable KO lines. Additionally, we successfully applied DIPA-CRISPR to aphids by inducing mutations via adult oviparous female injections in fertilized eggs. These robust genome-editing protocols will facilitate functional studies in aphids, a key model for research on evolution, ecology, development, and agriculture. Author SummarySurviving harsh winters is a challenge for many insects, and the production of specialized overwintering eggs is a common adaptation strategy. These eggs are protected from cold, desiccation, and fungal infections by their hardened, pigmented shells. The pea aphid, a hemipteran insect with a complex life cycle, relies on these eggs to survive winter. Aphids alternate between asexual reproduction in the warmer months and sexual reproduction in the fall, producing overwintering eggs that remain dormant until spring. In this study, we explored the role of Laccase2 (Lac2), a key gene that contributes to the strengthening and darkening of insect exoskeletons. We disrupted Lac2 in pea aphids using advanced genome-editing techniques, including a new approach called DIPA-CRISPR. This resulted in pigment-free eggs with weakened shells that were more prone to fungal infections and failed to hatch. This demonstrates that Lac2 is essential for the survival of overwintering eggs. In addition, we refined the CRISPR/Cas9 genome editing methods for pea aphids, enabling efficient and precise genetic studies. These findings and the tools we developed can facilitate research on ecology, evolution, and pest control, while shedding light on how insects adapt to challenging environments.

genetics↗

Maize rough endosperm6 is a predicted RNA helicase required for miRNA processing and endosperm cell patterning

Maize rough endosperm mutants have defective kernels with a rough, etched, or pitted endosperm surface. Molecular genetic analysis of this mutant class has identified multiple RNA processing proteins critical to endosperm development. Here, we report that rough endosperm6 (rgh6) encodes a predicted DEAD-box RNA helicase required for miRNA processing. Mutant rgh6 kernels reduce grain fill and increase relative transcript levels of markers specific to epidermal endosperm cell types. B-A translocation crosses revealed that rgh6 mutant endosperm inhibits normal embryo development. We mapped the rgh6 locus to a three gene interval and confirmed it encodes a predicted DEAD-box RNA helicase with two independent transposon-tagged alleles. Transient expression of a RGH6-green fluorescent protein (GFP) fusion is localized to nucleolus and nuclear speckles consistent with a function in nuclear RNA processing. Mutant rgh6 endosperms have increased precursor miRNA and decreased mature miRNA levels indicating that rgh6 impacts miRNA processing. Our study demonstrates that precursor miRNA processing and miRNA target regulation are required for normal endosperm development.

plant biology↗

Dynamic remodeling of mechano-sensing complexes in suspended fibroblast cell-sheets under external mechanical stimulus

Freestanding cell-sheets are valuable bio-materials for use in regenerative medicine and tissue engineering. Because cell-sheets experience various mechanical stimulations during handling, it is important to understand the responses of cells to these stimulations. Here, we demonstrate changes in the localization of various proteins during the stretching of fibroblast cell-sheets. These proteins are known to be involved in mechano-sensing. Upon stretching, actin filaments appear parallel to the stretching direction. At cell-cell junctions, {beta}-catenin forms clusters that co-localize with accumulated vinculin and zyxin as well as the actin filaments. The p130 Crk-associated substrate, known to be present in focal adhesions, is also recruited to these clusters and phosphorylated. Our results suggest that mechano-sensing machinery is formed at cell-cell junctions when the cell-sheets are stretched.

bioengineering↗

Proline-2'-deoxymugineic acid (PDMA) increases seed quality and yield by alleviating iron deficiency symptoms in soybean under calcareous-alkaline conditions

Iron (Fe) deficiency in crops, particularly in calcareous-alkaline soils, poses a major challenge due to Fe immobilization. While synthetic chelators like EDTA and EDDHA are commonly used to improve Fe availability, proline-2-deoxymugineic acid (PDMA) has emerged as a promising alternative, enhancing Fe nutrition in crops such as rice and cucumber. This study aimed to assess the effectiveness of PDMA on soybean growth and yield under calcareous-alkaline conditions. A pot trial demonstrated that PDMA improves Fe uptake, translocation, and storage in soybeans, leading to increased chlorophyll content, and enhanced root and shoot growth. Even at low dosages, PDMA significantly improved plant development, with the highest dosage (30 M) resulting in notable increases in Fe, Zn, Mn, and Mg concentrations in roots, leaves, and seeds, surpassing the effects of the synthetic chelator Fe-EDDHA in several parameters. Additionally, 30 M PDMA substantially boosted soybean yield, increasing pod and seed number, and 100-seed weight. It also improved seed quality by increasing protein and oil content. These findings suggest that PDMA offers a sustainable, effective alternative to traditional Fe chelators, providing a viable solution for addressing Fe deficiency and enhancing crop biofortification in challenging soil conditions.

plant biology↗

Serine chirality guides metabolic flow between one-carbon metabolism and neuromodulator synthesis

O_SCPLOWLC_SCPLOW-serine serves as a central metabolic node that integrates glycolytic flux, lipid metabolism, and one-carbon metabolism. In the mature central nervous system, O_SCPLOWLC_SCPLOW-serine is actively stereo-converted to O_SCPLOWDC_SCPLOW-serine, which functions as a neurotransmitter. However, the role of O_SCPLOWDC_SCPLOW-serine in cellular metabolism remains unclear. Here, we show that O_SCPLOWDC_SCPLOW-serine competes with mitochondrial O_SCPLOWLC_SCPLOW-serine transport, thereby suppressing one-carbon metabolism. Metabolomic analysis revealed that O_SCPLOWDC_SCPLOW-serine reduces intracellular glycine and formate levels, indicating inhibition of the initial step of the one-carbon pathway. Molecular dynamics simulations and enzymatic assays revealed that O_SCPLOWDC_SCPLOW-serine has low affinity for serine hydroxymethyltransferase 2 (Shmt2), which catalyzes the first step in mitochondrial one-carbon metabolism, and does not directly inhibit its activity. Instead, membrane transport assays demonstrated that O_SCPLOWDC_SCPLOW-serine competes with mitochondrial O_SCPLOWLC_SCPLOW-serine transport, depleting the substrate of Shmt2. Functionally, under O_SCPLOWLC_SCPLOW-serine poor conditions in vitro and ex vivo, O_SCPLOWDC_SCPLOW-serine inhibited the proliferation of immature and undifferentiated neural cells including glioblastoma stem cells, which depend highly on one-carbon metabolism. Notably, endogenous O_SCPLOWDC_SCPLOW-serine levels were low during early neurodevelopment, but increased with maturation, coinciding with a shift in the transcriptional profiles of serine metabolic enzymes at the cellular level. Given that O_SCPLOWLC_SCPLOW-serine supports neurodevelopment and O_SCPLOWDC_SCPLOW-serine modulates neurotransmission, this developmental shift in serine enantiomer metabolism appears to align with the functional transitions of the maturing nervous system. Thus, our findings reveal that serine chirality can influence mitochondrial substrate availability and one-carbon flux, offering previously unappreciated insight into the stereoselective regulation of cellular metabolism.

developmental biology↗

Mechanosensing by Piezo1 regulates osteoclast differentiation via PP2A-Akt axis in periodontitis

Mechanical stimulus to the multicellular bone unit (MBU) plays a key role in normal bone remodeling, whereas disuse osteoporosis, for example, represents loss of bone owing to lack of mechanical stresses. The analogy can be applied to a variety of pathogenic bone lytic complications, including periodontitis, in which local mechanical stress appears to be diminished. The activation of mechanosensitive Piezo1 Ca2+ channel expressed by osteoblasts and osteocytes in the MBU elicits the osteogenic signals in those cells. However, since osteoclast (OC)-specific Piezo1-gene knockout mice showed no skeletal phenotype, it has been assumed that Piezo1 might not play any role in OC-mediated bone remodeling. Here, however, we showed that mechanical stimulation of Piezo1 expressed on preosteoclasts (pre-OCs) downmodulates OC formation and, hence, bone resorptive activity in periodontitis, accompanied by significantly reduced expression of NFATc1, a master transcription factor for RANKL-induced OC-genesis. We know that the Ca2+/calcineurin/NFAT axis upregulates NFATc1 activation in pre-OCs. Interestingly, Piezo1-elicited Ca2+ influx did not affect NFATc1 expression. Instead, PP2A-mediated dephosphorylation of Akt downregulated NFATc1 in Piezo1-activated pre-OCs. However, systemic administration with Yoda1, a Piezo1 chemical agonist, or local injection of PP2A agonist, significantly downregulated the bone resorption induced in a mouse model of periodontitis, together with reduced numbers of TRAP+/phospho-Akt+ pre-OCs in local bone. These results suggest that mechanosensing by Piezo1 expressed on pre-OCs can downmodulate the RANKL-induced OC-genesis via the PP2A/Akt-dephosphorylation pathway, but that such Piezo1-mediated downregulation of bone resorption is attenuated in periodontitis. Significance StatementThe mechanosensitive Ca2+ channel Piezo1 plays important regulatory roles in a variety of cellular activities. RANKL-mediated OC-genesis requires permissive co-stimulatory signal from ITAM receptors, such as OSCAR and TREM2, to trigger the calcineurin/calmodulin signaling axis via Ca2+ oscillation, thereby upregulating NFATc1 expression. Activation of Piezo1 remarkably suppressed RANKL-induced NFATc1 activation which, in turn, reduced OC-genesis. Such mechanical activation of Piezo1 expressed on pre-OCs induced intracellular Ca2+ influx. Nonetheless, PP2A-mediated dephosphorylation of Akt, not the calcineurin/calmodulin pathway, suppressed NFATc1 in RANKL-elicited OC-genesis and resultant bone resorption, both in vitro and in vivo. These results indicate that mechanostress applied to pre-OCs can downregulate pathogenic OC-genesis and that Piezo1, as the mediator, is a novel molecular target for the development of anti-osteolytic therapies.

cell biology↗

INCOMPATIBILITY GROUPS OF PSEUDOMONAS PLASMIDS REVISITED: COMPREHENSIVE ANALYSIS OF R-FACTORS AND THEIR REPLICONS

Plasmids are the most influential engines of bacterial evolution and horizontal gene transfer, fueling the global spread of traits such as antimicrobial resistance. Their deep evolutionary relationships, however, remain difficult to resolve because current classification schemes are constrained by host range and nucleotide similarity. Replication initiation proteins (RIPs), which govern plasmid persistence and diversification, also remain poorly annotated across public databases. Here we establish PInc, a curated and experimentally grounded replicon classification framework anchored in historically defined incompatibility groups of Pseudomonas plasmids. Homology searches beyond PInc revealed that most replication initiators analyzed here share a conserved winged-helix (WH) domain, defining a broad WH RIP superfamily. Using the conserved WH region, we reconstructed a large-scale phylogeny that linked WH RIPs to over 100,000 plasmids, representing approximately half of those analyzed across public databases. This phylogeny resolved eight major clades and the deep split between the single- and double-winged-helix superclades, while revealing clade-specific host and environmental distributions and substantial RIP diversity not captured by current typing tools or annotation schemes. Together, these results overcome the historical host bias of plasmid typing and provide a replication-centered view of plasmid diversification across bacterial lineages and environments.

microbiology↗

PRDX6 dictates ferroptosis sensitivity by directing cellular selenium mobilization

Selenium-dependent glutathione peroxidase 4 (GPX4) is the guardian of ferroptosis and prevents unrestrained (phospho)lipid peroxidation by directly reducing phospholipid hydroperoxides (PLOOH) to their corresponding alcohols. However, it remains unclear whether other phospholipid peroxidases can also contribute to ferroptosis prevention, albeit to a varying degree. Here we show that cells lacking GPX4 still exhibit substantial PLOOH reduction capacity, arguing for the presence of alternative PLOOH peroxidases. By scrutinizing potential candidates, we showed that while overexpression of peroxiredoxin 6 (PRDX6), a thiol-specific antioxidant enzyme with reported PLOOH-reducing activity, failed to prevent ferroptosis, its genetic loss markedly sensitizes cancer cells to ferroptosis. Mechanistically, we uncover that PRDX6 facilitates intracellular selenium handling, which is crucial for selenium incorporation into selenoproteins, including GPX4. Consequently, PRDX6 modulates GPX4 expression, thereby dictating the sensitivity of cells to undergo ferroptosis. Our study highlights PRDX6 as a critical factor in ferroptosis prevention by directing cellular selenium mobilization.

cell biology↗