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Biology subjects

Tomita, T.

Publications and source records attributed to Tomita, T..

At least 19 recordsLinked to original sources

A plasma metabolomics workflow for breast cancer detection using quantitative GC/MS and machine learning

Blood-based metabolomic profiling has been widely investigated for breast cancer (BC) detection; however, clinical implementation remains limited due to variability in sample handling, analytical reproducibility, and overfitting during statistical analysis. We established a plasma GC/MS metabolomics workflow for discriminating BC from healthy controls (HC) using conventional machine-learning algorithms. Plasma samples (n = 360; BC = 180, HC = 180) were collected prospectively under standardized preanalytical conditions before surgery and the initiation of systematic anticancer therapy and analyzed using a quantitative GC/MS platform with automated derivatization. Feature selection and model development were conducted using three machine-learning (ML) algorithms (Lasso logistic regression (LR), random forest classifier (RFC), and support vector machine (SVM)). A total of 45 metabolite candidate biomarkers were identified, and the optimal number of metabolite features for each algorithm was estimated by a recursive feature elimination (RFE)-based strategy. The best-performing models achieved area under the ROC curve values (AUC) of 0.910 (LR), 0.893 (RFC), and 0.843 (SVM). We selected prioritizing candidate biomarkers consistently expressed across the multi-algorithm pipeline. A bagging ensemble model improved stability (AUC = 0.911) and reduced false-positive predictions in the independent HC dataset. In addition, model stability with respect to false-positive predictions was assessed using an independent HC cohort (n = 15) that was collected at a separate institution. These results indicate that a plasma metabolomics workflow combined with conventional multi-algorithm ML, algorithm-specific feature selection, and independent assessment provides stable discrimination between BC and HC in a moderately sized cohort.

cancer biology↗

XL-MS-Guided Structure Prediction of Disordered Encephalitozoon hellem Proteins

Microsporidia such as Encephalitozoon hellem are obligate intracellular human parasites that remain genetically intractable, limiting functional characterization of their proteomes. Structural studies based on homology-based modeling and the use of deep learning algorithms of microsporidian proteins also remain limited because most have little to no sequence similarity to proteins with solved structures. To address these limitations, we developed an approach that incorporates cross-linking mass spectrometry (XL-MS) data into structure prediction. XL-MS data provides upper bound distance constraints that can be incorporated into protein deep-learning based modeling and subsequent docking. Using this approach, we generated a model for two interacting E. hellem spore wall proteins Spore Wall Protein 1B (Swp1b) and Endospore Protein 1 (EnP1), with no clear homologs outside of microsporidia, and which contain several disordered regions. These proteins are extremely abundant spore wall proteins of microsporidia and previously were not known to interact with one another. The resulting model not only is consistent with the experimental crosslinks used to generate the model but was subsequently confirmed by independently generated XL-MS data. The described AlphaLink-Modeller framework for structure prediction is particularly well suited to proteins with limited homology and/or substantial flexible regions, given they adopt a defined structural state within a biological context, thereby extending integrative modeling approaches to previously inaccessible targets.

microbiology↗

Subtype-specific secretion of extracellular vesicles by LRRK2 and Rab GTPases under lysosomal stress

LRRK2, the Parkinsons disease-associated kinase, phosphorylates a subset of Rab GTPases and regulates membrane dynamics. We previously reported that lysosomal stress activates LRRK2 and thereby induces the exocytic secretion of lysosomal contents, but the detailed secretion mechanism remained unclear. Here we found that, under lysosomal stress, endolysosomal luminal and membrane components were secreted with extracellular vesicles (EVs) via LRRK2. Bis(monoacylglycerol)phosphate, an endolysosomal lipid and a urinary marker of LRRK2 activity, was similarly secreted via LRRK2, whereas CD9-positive EVs were not involved. Further dissection of the secreted EVs revealed that Alix-positive EVs were secreted via Rab8a as well as the ESCRT component VPS4, whereas LAMP1/cathepsin B-positive EVs were secreted via Rab10/Rab35, and SNARE proteins syntaxin 2 and VAMP8 regulated the secretion of both EV subtypes. These findings suggest a distinctive stress-induced secretory mechanism whereby LRRK2 facilitates the secretion of multiple EV subtypes by controlling Rab GTPases involved in each pathway.

cell biology↗

Cryo-EM structure of pro-aggregant P301L/S320F double-mutant tau filaments formed in mouse brains following peripheral AAV delivery

Tauopathies are characterized by the accumulation of abnormally phosphorylated tau filaments, with disease-specific folds revealed by cryo-electron microscopy (cryo-EM). Here, we delivered a recombinant human tau carrying the P301L/S320F double mutation into AppNL-G-F/MAPT double knock-in mice using a blood-brain-barrier-permeable AAV (AAV-PHP.eB), enabling rapid induction of tau aggregation in vivo. The mutant tau was systemically administered via retro-orbital injection, providing a minimally invasive approach for widespread neuronal transduction. Phosphorylated tau aggregation, as well as seeding activity, were observed without the need for exogenous seeds. Our cryo-EM analysis resolved a novel filament fold incorporating residues 279-329, in which the P301L and S320F mutations introduced stabilizing interactions that reinforced filament assembly. This conformation was distinct from previously reported folds, including Alzheimer and Pick tau filaments. Moreover, the filaments adopted a more compact architecture than those observed in patient-derived samples or other model mice. This finding demonstrates that P301L/S320F double-mutant tau adopts a structurally unique, highly aggregation-prone fold, and that this system provides a rapid platform for modeling tau filament formation.

neuroscience↗

Aging disrupts tissue homeostasis and constrains blastema-mediated regeneration in the Cladonema medusa

Regenerative capacity varies widely across animals, yet aging is often accompanied by declining tissue homeostasis and regenerative potential. In many species, regeneration of complex structures relies on epimorphic programs that form a blastema, coordinating cell proliferation and pattern reorganization after injury. Although aging-associated regeneration defects have been documented in several bilaterian models, how aging shapes regeneration in early-branching metazoans with robust regenerative abilities remains unclear. Here, we investigate aging and regeneration in the medusa stage of Cladonema pacificum, a cnidarian that retains high regenerative capacity within a finite lifespan. We show that aging in Cladonema medusae is accompanied by progressive morphological and functional deterioration, including shrinkage of the umbrella and manubrium, tentacle shortening, and reduced reproductive output, along with increased DNA damage. At the cellular level, aging is associated with depletion of differentiated cell populations, including nematocytes and neurons, as well as reductions in stem cell-associated populations and proliferative activity in the tentacle bulb. Consistent with these changes, tentacle regeneration is markedly impaired in aged medusae and is characterized by delayed wound closure, defective blastema formation, and incomplete functional recovery. Together, our findings indicate that aging disrupts both tissue homeostasis and blastema-mediated regeneration in Cladonema medusae, establishing a tractable model for studying aging-regeneration interactions and supporting the view that aging imposes broadly shared constraints on regenerative systems across metazoans.

developmental biology↗

Caveolin-1 controls lineage fidelity of adult neural stem cells via lysosomal degradation of PDGFRα

Caveolae are cell-surface signaling hubs involved in stem cell proliferation and differentiation. However, the molecular details of how they influence stem cell quiescence remain poorly understood. In this study, we show that most caveolae components, particularly caveolin-1 (Cav-1), are specifically upregulated in quiescent neural stem cells (NSCs). Furthermore, we demonstrate that Cav-1 restricts platelet-derived growth factor receptor (PDGFR) signaling, a key regulator for NSC proliferation and oligodendrocyte differentiation in the adult brain, through lysosomal degradation. Genetic ablation of Cav-1 leads to aberrant NSC activation, reduced neurogenesis, and enhanced ectopic oligodendrocyte differentiation on the ventricular surface in the ventral side of the ventricular-subventricular zone (V-SVZ), a key NSC niche responsible for neuroblast differentiation. Mechanistically, we show that Cav-1 deficiency suppresses the endo-lysosomal degradation of PDGFR, leading to PDGFR accumulation and excessive signaling for oligodendrocyte differentiation. Taken together, our results uncover a crucial homeostatic mechanism wherein caveolae function as a safeguard to maintain adult NSC quiescence and lineage fidelity by controlling lysosomal turnover of PDGFR in a niche-specific manner.

neuroscience↗

Catalytic regulation of CoA transferase by an NAD+-sensing accessory protein and protein acetylation

CoA transferases play essential roles in short-chain fatty acid metabolism by catalyzing the reversible transfer of CoA groups between acyl substrates. However, how their activities are regulated in response to cellular metabolic states remains unclear. Here we identify a dual regulatory mechanism of a CoA transferase from Thermus thermophilus, which is controlled by both interaction with an NAD+-sensing accessory protein and protein acetylation. The enzyme associates with an alanine dehydrogenase-like protein that lacks catalytic activity but binds NAD+ and NADH. Biochemical analyses revealed that inhibition occurs specifically upon NAD+ binding, but not NADH, indicating that the alanine dehydrogenase-like protein senses the intracellular NAD+/NADH ratio. Cryo-electron microscopy structures of the complex of CoA transferase and alanine dehydrogenase-like protein reveal the structural basis of this redox-dependent inhibition. Furthermore, acetylation of the CoA transferase alleviates the inhibition. Since the NAD+/NADH ratio and acetyl-CoA levels reflect the cellular energy and metabolic states, these findings uncover a previously unrecognized regulatory link through which redox sensing and acetylation cooperate to fine-tune the {beta}-oxidation flux.

biochemistry↗

Intrinsic and TDP-43 dysfunction-induced catabolic stress elicit neuroprotective cellular degradation in ALS-vulnerable motor neurons

Selective neuronal vulnerability is a defining feature of neurodegenerative disorders, exemplified by motor neuron degeneration in amyotrophic lateral sclerosis (ALS). The nature of motor neurons underlying this selectivity remains unresolved. Here, by monitoring autophagy at single-cell resolution across the translucent zebrafish spinal cord, we identify motor neurons as the cell population with the highest autophagic flux. Large spinal motor neurons (SMNs), most susceptible to ALS, exhibit higher flux compared to smaller SMNs and ALS-resistant ocular motor neurons. Notably, large SMNs accelerates both autophagy and proteasome-mediated degradation, which are further augmented by TDP-43 loss. Additionally, acceleration of multiple unfolded protein response pathways indicates their innate tendency to accumulate misfolded proteins. Enhanced cellular degradation in large SMNs is neuroprotective as its inhibition halts axon outgrowth. These findings propose that cell size-associated degradation load underlies selective neuronal vulnerability in ALS, highlighting the alleviation of catabolic stress as a target of therapy and prevention.

neuroscience↗

Mapping a Toxoplasma gondii interactome by crosslinking mass spectrometry and machine learning

Toxoplasma gondii, a widespread human parasite, persists in hosts through complex molecular interactions. Protein-protein interactions (PPIs) underpin essential biological processes, including parasite-host interactions and cellular invasion. Herein, we utilized advanced crosslinking mass spectrometry (XL-MS) techniques to map a T. gondii tachyzoite cytosolic extract interactome. By integrating MS-cleavable and non-cleavable analysis, we identified a total of 405 unique PPIs at medium confidence (FDR < 5%) and 226 at high confidence (FDR < 1%), revealing both known and novel interactions within critical cellular complexes such as the ribosome, proteasome, and dense granule proteins. Structural validation confirmed spatial proximity of crosslinked residues, while comparative analyses against existing datasets (hyperLOPIT, ToxoNET, STRING) corroborated the biological relevance of identified interactions. Furthermore, we introduced a machine learning approach leveraging biological annotations and experimental data to significantly enhance the detection and validation of PPIs. Our findings not only provide a refined view of T. gondiis molecular architecture, but also highlight the utility of XL-MS coupled with computational tools in dissecting complex parasite proteomes. The XL-MS interactome map provides a new valuable resource for understanding parasite biology and developing targeted therapeutic strategies.

microbiology↗

Editing of the polyubiquitin architecture on the collided ribosome maintains persistent RQC activity

In Ribosome-associated Quality Control (RQC), K63-linked polyubiquitination of uS10 on the stalled ribosome is crucial for recruiting the RQC-trigger (RQT) complex. However, the mechanisms governing the maintenance and recycling of polyubiquitin architecture on colliding ribosomes remain unclear. Here we demonstrate that two deubiquitinating enzymes (DUBs), Ubp2 and Ubp3, play key roles in editing and recycling polyubiquitin chains on uS10, thereby contributing to the promotion of RQC activity. Specifically, Ubp2 eliminates the K63-linked polyubiquitin chain from uS10 on the free 40S subunit for recycling, while Ubp3 predominantly cleaves the K48-linked di-ubiquitin and the K48/K63-mixed-linkage poly-ubiquitin chain from uS10 on the translating ribosomes. Notably, we further demonstrate that the ubiquitin chains containing K48-linkage of the uS10 on the colliding ribosome act as a negative signal for the RQT-mediated ribosome dissociation process. Collectively, our findings clarify the ubiquitin code in RQC and define the positive functions of these two DUBs in maintaining the persistent RQC activity.

molecular biology↗

Development of CRISPR/Cas13-based analytical tools to study RNA-Protein Interactions

RNA-protein interactions (RPIs) are as important as protein-protein interactions (PPIs) for the formation of membraneless organelles (MLOs) and play a vital role in various biological processes. Despite remarkable advances in PPI analysis technologies in recent years, the development of RPI analysis tools has lagged behind. To advance RPI analysis, we integrated three established PPI tools--bimolecular fluorescence complementation (BiFC), NanoBiT, and split-TurboID--with the RNA-targeting CRISPR/Cas13. We applied these tools to analyze paraspeckles, one of the best known MLOs formed by interactions between the long non-coding RNA NEAT1 and the RNA-binding protein NONO. The optimized BiFC-dCas13 allows live cell imaging and quantitative detection of the NEAT1-NONO interaction. The NanoBiT-dCas13 detects dynamic changes in the NEAT1-NONO interaction in an immediate and reversible manner. As a proximity labeling tool, the Split-TurboID-dCas13 induces biotinylation of proteins surrounding paraspeckles, leading to the identification of the N6-methyladenosine reader protein YTHDC1 as a novel paraspeckles-associated protein. The BiFC-dCas13, NanoBiT-dCas13, and Split-TurboID-dCas13 systems have a broad utility for the analysis of RPIs and MLOs.

bioengineering↗

Inhibition of NF-κB signaling pathway in astrocytes facilitates amyloid-β clearance by kallikrein-related peptidase 7

Alzheimer disease (AD) is characterized by the deposition of amyloid-{beta} peptide (A{beta}). Decreased A{beta} clearance is observed in sporadic AD patients, suggesting that enhancing A{beta} clearance is a potential therapeutic approach for AD. We identified kallikrein-related peptidase 7 (KLK7) as an astrocyte-derived A{beta}-degrading protease, and its mRNA expression is reduced in AD brains. Memantine, an N-methyl-D-aspartate (NMDA) receptor antagonist, upregulates KLK7 expression in astrocytes; however, the regulatory mechanism remains unclear. Here, we show that the NMDA receptor signaling negatively regulates KLK7 mRNA expression via nuclear factor-{kappa}B (NF-{kappa}B). Inhibition of NF-{kappa}B signaling pathway in astrocytes increases KLK7 expression and promotes A{beta} degradation. Moreover, the mRNA expression level of the NF-{kappa}B family is elevated in AD brains and shows a negative correlation with KLK7 mRNA expression. Finally, the injection of an NF-{kappa}B inhibitor significantly upregulates Klk7 expression and reduces A{beta} levels in vivo. These findings suggest that the NMDA receptor-NF-{kappa}B signaling axis in astrocytes negatively regulates KLK7 expression and modulates KLK7-mediated A{beta} clearance.

neuroscience↗

Aggregation of HAPLN2, a component of the perinodal extracellular matrix, is a hallmark of physiological brain aging in mice

Protein aggregation is a hallmark of neurodegenerative diseases and is also observed in the brains of elderly individuals without such conditions, suggesting that aging drives the accumulation of protein aggregates. However, the comprehensive understanding of age-dependent protein aggregates involved in brain aging remains unclear. Here, we investigated proteins that become sarkosyl-insoluble with age and identified hyaluronan and proteoglycan link protein 2 (HAPLN2), a hyaluronic acid-binding protein of the extracellular matrix at the nodes of Ranvier, as an age-dependent aggregating protein in mouse brains. Elevated hyaluronic acid levels and impaired microglial function reduced the clearance of HAPLN2, leading to its accumulation. HAPLN2 oligomers induced microglial inflammatory responses both in vitro and in vivo. Furthermore, age-associated HAPLN2 aggregation was also observed in the human cerebellum. These findings suggest that HAPLN2 aggregation results from age-related decline in brain homeostasis and may exacerbate the brain environment by activating microglia. This study provides new insights into the mechanisms underlying cerebellar aging and highlights the role of HAPLN2 in age-associated changes in the brain. Author SummaryTo identify age-dependent protein aggregates unrelated to disease, we analyzed the sarkosyl-insoluble proteome of young and aged mouse brains. We discovered that hyaluronan and proteoglycan link protein 2 (HAPLN2), a hyaluronic acid-binding protein existing in the nodal extracellular matrix, accumulated with age. Age-dependently accumulated HAPLN2 formed large protein aggregates that cannot be solubilized by the anionic detergent sarkosyl or by hyaluronidase digestion. In addition, HAPLN2 formed irregularly shaped puncta that were mislocalized from the nodes of Ranvier in the cerebellar white matter of not only aged mice but also aged human brains. Oligomers of full-length HAPLN2 specifically induced microglial activation in vitro and in vivo. Our findings suggest that the accumulation of HAPLN2 aggregates is a new hallmark of brain aging and a possible factor contributing to brain inflammation.

biochemistry↗

Selective agonism of GPR34 stimulates microglial uptake and clearance of amyloid β fibrils

Microglia, the primary immune cells of the central nervous system, play a crucial role in maintaining brain homeostasis through phagocytosis of various substrates, including amyloid-{beta} (A{beta}) fibrils, a hallmark of Alzheimer disease (AD) pathology. However, the molecular mechanisms regulating microglial A{beta} uptake remain poorly understood. Here, we identified GPR34, a Gi/o-coupled receptor highly expressed in microglia, as a novel regulator of fibrillar A{beta} phagocytosis. Treatment with a selective GPR34 agonist, M1, specifically enhanced uptake of A{beta} fibrils, but not its monomer or oligomer, in both mouse and human microglia. Mechanistically, M1 reduced intracellular cAMP levels, which inversely correlated with A{beta} uptake activity. Importantly, a single intrahippocampal injection of M1 in an AD mouse model significantly increased microglial A{beta} uptake in vivo. Furthermore, single-nucleus RNA-sequencing analysis of Japanese AD patient samples revealed a significant reduction of GPR34 expression in microglia from AD patients compared to controls. We also observed an age-dependent decline in microglial GPR34 expression in both human and mouse datasets, suggesting a potential contribution of GPR34 downregulation to age-related A{beta} accumulation and AD risk. Collectively, our findings identify GPR34 as a promising target for modulating microglial A{beta} clearance and highlight the therapeutic potential of GPR34 agonists in AD. Significance statementAlzheimer disease (AD) is characterized by amyloid-{beta} (A{beta}) accumulation in the brain. Microglia, the brains immune cells, play a crucial role in the metabolism of A{beta}. We discovered that activating the microglial receptor GPR34 with a selective agonist enhances the phagocytosis of A{beta} fibrils, a key pathogenic form of A{beta}. Importantly, GPR34 expression decreases with aging and AD progression, potentially contributing to impaired A{beta} clearance. Our findings highlight GPR34 as a promising therapeutic target for AD, as boosting its activity could promote A{beta} clearance and slow disease progression. This study provides valuable insights into microglial function in AD and offers a novel strategy for developing disease-modifying therapies.

neuroscience↗

A Toxoplasma gondii O-glycosyltransferase that modulates bradyzoite cyst wall rigidity is structurally and functionally distinct from host homologues

Infection with the Apicomplexan protozoan Toxoplasma gondii can be life-threatening in immunocompromised hosts. Transmission frequently occurs through the oral ingestion of T. gondii bradyzoite cysts, which transition to tachyzoites, disseminate, and then form cysts containing bradyzoites in the central nervous system, resulting in latent infection. There are currently no effective treatments to cure latent infection. Bradyzoites are encapsulated by a cyst wall that is critical for immune evasion, survival, and transmission. Cyst wall rigidity is influenced by the O-glycosylation of the mucin domain of the cyst wall protein CST1 by mucin-type O-glycosyltransferases (GalNAc-Ts). Here, we report the first structures of a protozoan GalNAc-T, T.gondii-GalNAc-T3 in the apo state and in complex with glycopeptide substrates. The structures reveal features that are strictly conserved in Apicomplexan homologues of T.gondii-GalNAc-T3, including a unique 2nd metal binding site that is coupled to substrate binding and enzymatic activity in vitro and cyst wall O-glycosylation in T. gondii. Additional structural features illustrate the divergence of GalNAc-Ts from parasite to host and highlight multiple druggable sites in T.gondii-GalNAc-T3 and its homologues in Apicomplexa that are responsible for a wide range of parasitic diseases.

biochemistry↗

Cryo-EM structures of tau filaments from SH-SY5Y cells seeded with brain extracts from cases of Alzheimer's disease and corticobasal degeneration

The formation of amyloid filaments through templated seeding is believed to underlie the propagation of pathology in most human neurodegenerative diseases. A widely used model system to study this process is to seed amyloid filament formation in cultured cells using human brain extracts. Here, we report the electron cryo-microscopy (cryo-EM) structures of tau filaments from undifferentiated seeded SH-SY5Y cells, that transiently expressed N-terminally HA-tagged 1N3R or 1N4R human tau, using brain extracts from individuals with AD or CBD. Although the resulting filament structures differed from those of the brain seeds, some degree of structural templating was observed. Studying templated seeding in cultured cells, and determining the structures of the resulting filaments, can thus provide insights into the cellular aspects underlying neurodegenerative diseases.

neuroscience↗

Exploring the genetic diversity of the Japanese Population: Insights from a Large-Scale Whole Genome Sequencing Analysis

The Japanese archipelago is a terminal location for human migration, and the contemporary Japanese people represent a unique population whose genomic diversity has been shaped by multiple migrations from Eurasia. Through high-coverage whole-genome sequencing (WGS) analysis of 9,850 samples from the National Center Biobank Network, we analyzed the genomic characteristics that define the genetic makeup of the modern Japanese population from a population genetics perspective. The dataset comprised populations from the Ryukyu Islands and other parts of the Japanese archipelago (Hondo). Low frequency detrimental or pathogenic variants were found in these populations. The Hondo population underwent two episodes of population decline during the Jomon period, corresponding to the Late Neolithic, and the Edo period, corresponding to the Early Modern era, while the Ryukyu population experienced a population decline during the shell midden period of the Late Neolithic in this region. Genes related to alcohol and lipid metabolism were affected by positive natural selection. Two genes related to alcohol metabolism were found to be 12,500 years out of phase with the time when they began to be affected by positive natural selection; this finding indicates that the genomic diversity of Japanese people has been shaped by events closely related to agriculture and food production. Author summaryThe human population in the Japanese archipelago exhibits significant genetic diversity, with the Ryukyu Islands and other parts of the archipelago (Hondo) having undergone distinct evolutionary paths that have contributed to the genetic divergence of the populations in each region. In this study, whole genome sequencing of healthy individuals from national research hospital biobanks was utilized to investigate the genetic diversity of the Japanese population. Haplotypes were inferred from the genomic data, and a thorough population genetic analysis was conducted. The results indicated not only genetic differentiation between Hondo and the Ryukyu Islands, but also marked differences in past population size. In addition, gene genealogies were inferred from the haplotypes, and the patterns were scrutinized for evidence of natural selection. This analysis revealed unique traces of natural selection in East Asian populations, many of which were believed to be linked to dietary changes brought about by agriculture and food production.

genomics↗

Evolutionarily acquired activity-dependent transformation of the CaMKII holoenzyme

Ca2+/calmodulin-dependent protein kinase II (CaMKII) has long been central in synaptic plasticity research. CaMKII is a dodecameric serine/threonine kinase that has been essentially conserved across metazoans for over a million years. While the mechanisms of CaMKII activation are well studied, its "behavior" at the molecular level has remained unobserved. Here, high-speed atomic force microscopy was used to visualize the activity-dependent structural dynamics of rat/hydra/C. elegans CaMKII in various states at nanometer resolution. Among the species, rat CaMKII underwent internal kinase domain aggregation in an activity-dependent manner and showed a higher tolerance to dephosphorylation by phosphatase. Our findings suggest that mammalian CaMKII has evolutionarily acquired a new structural form and a tolerance to phosphatase to maintain robust CaMKII activity for proper neuronal function. One-Sentence SummaryHigh-speed atomic force microscopy reveals the activity-dependent structural dynamics of rat/hydra/C. elegans CaMKII

neuroscience↗