eLife最新文献

{"title":"A framework for analyzing global <i>Caenorhabditis elegans</i> neural activity.","authors":"Iulia Rusu, Zachary T Cecere, Javier J How, Kathleen T Quach, Eviatar Yemini, Tatyana O Sharpee, Sreekanth H Chalasani","doi":"10.7554/eLife.108234","DOIUrl":"https://doi.org/10.7554/eLife.108234","url":null,"abstract":"<p><p>Neurons represent changes in external and internal environments by altering their activity patterns. While coherent brain-wide patterns of neural activity have been observed in neuronal populations, very little is known about their dimensionality, geometry, and how they are correlated with sensory inputs. Here, we recorded the activity of most head neurons in <i>Caenorhabditis elegans</i> experiencing changes in bacterial or control buffer stimuli around their nose. We first classified active neurons into six functional clusters: two sensory neuron clusters (ON and OFF responding to addition and removal of stimuli, respectively) and four motor/command neuron clusters (AVA, RME, SMDD, and SMDV). Next, we estimated stimulus selectivity for each cluster and found that while sensory neurons exhibit their maximal responses within 15 s, changes in bacterial stimuli drive maximal responses in command and motor neuron clusters after tens of seconds. Furthermore, we show that bacterial stimuli induce neural dynamics that are best described by a hyperbolic, not Euclidean, space indicating hierarchical organization in <i>C. elegans</i> neural population dynamics. This space was 8-dimensional, with dimensions that aligned in one sensory direction (ON and OFF neurons), two motor directions (forward-backward and dorsal-ventral), and the rest of dimensions corresponding with unclassified neurons. Collectively, we show that <i>C. elegans</i> neural activity can be effectively represented in low-dimensional hyperbolic space and describe how sensory information is processed by the neural network.</p>","PeriodicalId":11640,"journal":{"name":"eLife","volume":"15 ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13661047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endosome-associated Rab GTPases control distinct aspects of neural circuit assembly.","authors":"Katherine X Dong, Yanbo Zhang, Hui Ji, David J Luginbuhl, Liqun Luo, Colleen N McLaughlin","doi":"10.7554/eLife.109394","DOIUrl":"10.7554/eLife.109394","url":null,"abstract":"<p><p>Neural circuit assembly relies on the precise regulation of cell-surface receptors that mediate signaling and adhesion. Endocytosis controls receptor activity and availability by internalizing and routing proteins through early endosomes to one of two main pathways: recycling back to the cell-surface or delivery to lysosomes for degradation. Rab GTPases direct receptors into these distinct pathways, but their specific contributions to circuit formation remain opaque. Using clonal analyses with null alleles, we dissected the roles of Rab-mediated trafficking to early, late, and recycling endosomes across multiple stages of circuit assembly <i>in vivo.</i> Our approach revealed that Rab5 and Rab11 regulate extensive and largely distinct developmental events, highlighting the pivotal roles of early endosome sorting and recycling pathways in circuit assembly. As neurons mature, both the spatial distribution and abundance of specific endocytic compartments change to reflect evolving trafficking demands. Our findings underscore how distinct post-endocytic trafficking fates are necessary to build neural circuits.</p>","PeriodicalId":11640,"journal":{"name":"eLife","volume":"14 ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13661049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synaptic vesicle undocking induces low-frequency depression.","authors":"Melissa Silva, Federico F Trigo, Isabel Llano, Alain Marty","doi":"10.7554/eLife.110329","DOIUrl":"10.7554/eLife.110329","url":null,"abstract":"<p><p>Synaptic depression is often interpreted as reflecting depletion of the readily releasable pool (RRP) following exocytosis. Such a mechanism predicts little or no depression at low stimulation frequency, as RRP replenishment should then offset the loss of vesicles by exocytosis. Nevertheless, in several types of mammalian central synapses, repetitive presynaptic stimulation at low frequency (<5 Hz) elicits synaptic depression (low-frequency depression or LFD). In the present work, we count the number of synaptic vesicles released at individual active zones to study the RRP and its replenishment during LFD. Contrary to depletion models of synaptic depression, we find that LFD does not depend on previous SV consumption. We find that LFD displays a long recovery time course (tens of seconds) when challenged by isolated stimulations but is immediately reversed by a high-frequency train. We suggest that LFD results from undocking, a shift between two classes of synaptic vesicles organized sequentially inside the RRP (replacement vs. docked vesicles) in favor of the upstream (replacement) state. To explain the dependence of LFD recovery on stimulation frequency, we propose that, while undocking is apparent hundreds of milliseconds after a stimulation, calcium-dependent docking takes only a couple of milliseconds. Consistent with the undocking model, we find that double presynaptic stimulations alleviate LFD as they favor vesicular docking and RRP replenishment. Finally, we expand our model to explain how stimulation frequency shapes short-term synaptic depression, changing from depression at low frequency to a facilitation-depression sequence at medium- or high-frequency trains.</p>","PeriodicalId":11640,"journal":{"name":"eLife","volume":"15 ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13657630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome-wide mapping of Cas9-induced sister chromatid exchange across single and over 200 genomic sites in human cells.","authors":"Peter Chovanec, Shiyang He, Yi Yin","doi":"10.7554/eLife.112073","DOIUrl":"10.7554/eLife.112073","url":null,"abstract":"<p><p>CRISPR/Cas9-induced DNA double-strand breaks (DSBs) are widely used for genome engineering, yet their capacity to provoke sister chromatid exchange (SCE) remains incompletely understood because exchanges between identical sisters leave no sequence change and are invisible to conventional sequencing. Using sci-L3-Strand-seq, a scalable single-cell template-strand sequencing platform, we mapped SCE following targeted Cas9 cleavage. Cas9 targeting of a unique genomic locus strongly enriched SCE at the break site, reaching 41% in the same cell cycle and 17% in the subsequent division, indicating frequent non-local inter-sister repair. Targeting 237 repetitive Alu sites produced mild enrichment of on-target SCE, whereas cells with elevated SCE burden showed significant enrichment at programmed cut sites, suggesting context-dependent recombination at repetitive loci. Reciprocal daughter-cell pair analysis revealed large-scale structural alterations on chromosomes with induced SCEs and at SCE junctions, indicating that Cas9-induced SCE does not universally reflect error-free homologous recombination. Disruption of LIG3, LIG4, XRCC1, and XRCC4 at Cas9 cut sites did not measurably alter SCE frequency, consistent with delayed functional loss following editing. Together, these findings identify Cas9-induced DSBs as potent local triggers of SCE and reveal structural outcomes invisible to conventional sequencing.</p>","PeriodicalId":11640,"journal":{"name":"eLife","volume":"15 ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13657629/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149167312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synaptic connectome of a neurosecretory network in the <i>Drosophila</i> brain.","authors":"Theresa H McKim, Jayati Gera, Ariana J Gayban, Kevin Christie, Joel Shin, Nils Reinhard, Giulia Manoli, Selina Hilpert, Patrick Callaerts, Floris van Breugel, Charlotte Helfrich-Förster, Meet Zandawala","doi":"10.7554/eLife.102684","DOIUrl":"10.7554/eLife.102684","url":null,"abstract":"<p><p>Hormones mediate inter-organ signaling, which is crucial in orchestrating diverse behaviors and physiological processes, including sleep and activity, feeding, growth, metabolism, and reproduction. The pars intercerebralis and pars lateralis in insects represent major hubs that contain neurosecretory cells (NSCs) that produce various peptide hormones. To obtain insight into how hormonal signaling is regulated, we have characterized the synaptic connectome of NSCs in the adult <i>Drosophila</i> brain. Identification of neurons providing inputs to multiple NSC classes implicates diuretic hormone 44-expressing NSCs as a major coordinator of physiology and behavior. Surprisingly, despite most NSCs having dendrites in the subesophageal zone (primary taste processing center), inputs from peripheral gustatory neurons to NSCs are largely indirect. We also deciphered pathways via which diverse olfactory inputs are relayed to NSCs. Using an influence metric, based on a linear dynamical systems approach, we identify enteric neurons as the strongest influencers of NSC activity compared to other sensory modalities. Further, our analyses revealed substantial inputs from brain descending neurons to NSCs, suggesting that descending neurons regulate both endocrine and motor output to synchronize physiological changes with appropriate behaviors. In contrast to NSC inputs, synaptic output from NSCs is sparse and mostly mediated by corazonin NSCs. We show that both corazonin-expressing NSCs and their downstream synaptic partner DNg27 influence egg-laying. We additionally explore putative paracrine interconnectivity between NSC classes and peptide hormone pathways from NSCs to peripheral tissues by analyzing single-cell transcriptomic datasets. Our comprehensive characterization of the <i>Drosophila</i> neurosecretory network connectome provides a platform to understand complex hormonal networks and how they orchestrate animal behaviors and physiology.</p>","PeriodicalId":11640,"journal":{"name":"eLife","volume":"13 ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13657632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Svep1 orchestrates distal airway patterning and alveolar differentiation in murine lung development.","authors":"Nicole Foxworth, Julie Wells, Sara Ocana-Lopez, S Muller, Pooja Bhayani, James Denegre, Kristina Palmer, Wendy Memishian, Teresa McGee, Stephen A Murray, Patricia K Donahoe, Carol J Bult, Maria Loscertales","doi":"10.7554/eLife.100443","DOIUrl":"10.7554/eLife.100443","url":null,"abstract":"<p><p>Disruptions in airway branching or alveolar differentiation during lung development can lead to severe respiratory deficiencies and neonatal death. The molecular mechanisms governing branching patterning and early alveolar formation remain elusive. Loss of <i>Svep1</i> function in mice results in various developmental defects, including lung hypoplasia and perinatal lethality. Our examination of the lungs of <i>Svep1</i> knockout (<i>Svep1^-/-</i>) mouse embryos, both in vivo and in vitro, revealed that <i>Svep1</i> mutants exhibit an increase in the number of disorganized distal airway tips, progressively greater disruption of lung lobe morphology over time, and disrupted saccular development. <i>Svep1</i> interacts with FGF signaling to regulate smooth muscle differentiation and, together with <i>Fgf9</i>, guides airway branching patterning. Transcriptomic data from the lungs of <i>Svep1^-/-</i> embryos revealed dysregulated gene expression affecting saccular maturation. Our findings demonstrate that <i>Svep1</i> is a key extracellular matrix player shaping airway morphology and influencing alveolar fate. These insights offer potential avenues for therapeutic interventions in congenital lung disorders.</p>","PeriodicalId":11640,"journal":{"name":"eLife","volume":"13 ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13657628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Product-stabilized filamentation by human glutamine synthetase allosterically tunes metabolic activity.","authors":"Eric Greene, Richard Muniz, Hiroki Yamamura, Samuel E Hoff, Priyanka Bajaj, Markus C B Tecson, Cyrina Geluz, D John Lee, Erin M Thompson, Angelika Arada, Gyun Min Lee, Massimiliano Bonomi, Justin M Kollman, James S Fraser","doi":"10.7554/eLife.108336","DOIUrl":"10.7554/eLife.108336","url":null,"abstract":"<p><p>To maintain metabolic homeostasis, enzymes must adapt to fluctuating nutrient levels through mechanisms beyond gene expression. Here, we demonstrate that human glutamine synthetase (GS) can reversibly polymerize into filaments aided by a composite binding site formed at the filament interface by the product, glutamine. Time-resolved cryo-electron microscopy (cryo-EM) confirms that glutamine binding stabilizes these filaments, which in turn exhibit reduced catalytic specificity for ammonia at physiological concentrations. This inhibition appears induced by a conformational change that remodulates the active site loop ensemble gating substrate entry. Metadynamics ensemble refinement revealed >10 Å conformational range for the active site loop and that the loop is stabilized by transient contacts. This disorder is significant, as we show that the transient contacts which stabilize this loop in a closed conformation are essential for catalysis both in vitro and in cells. We propose that GS filament formation constitutes a negative-feedback mechanism, directly linking product concentration to the structural and functional remodeling of the enzyme.</p>","PeriodicalId":11640,"journal":{"name":"eLife","volume":"14 ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13657631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Robust and replicable effects of ageing on resting-state brain electrophysiology measured with MEG.","authors":"Andrew J Quinn, Jemma Pitt, Oliver Kohl, Chetan Gohil, Mats W J van Es, Anna C Nobre, Mark W Woolrich","doi":"10.7554/eLife.108829","DOIUrl":"10.7554/eLife.108829","url":null,"abstract":"<p><p>Non-invasive recordings of brain electrophysiology provide credible insights into decline in neuronal functioning with age. New approaches are required to translate these results into compelling clinical metrics and meet the global challenge of preserving brain health in ageing. Changes in neuronal dynamics with ageing are observable in the power spectra of EEG and MEG recordings. Highly promising candidates for electrophysiological markers have been identified, but progress is hindered by substantial methodological variability across studies. This makes it challenging to establish a clear consensus on the frequency, location, and direction of any single reported effect within the larger body of research. We estimate a full-frequency whole-head profile of the ageing effect on eyes-closed resting-state MEG using the GLM-Spectrum. This data representation is easily sharable, facilitates meta-analyses, and provides a framework for estimating statistical power of age effects for future study planning. We use this to show that the effect of age replicates across open-access MEG datasets and is robust to modelling of common covariates. Distinct components within the full-frequency profile have different effect sizes, indicating that sample-size planning for ageing effects must consider the specific features of interest. The frequency profile of ageing is strongly robust to a range of common covariates and partially robust to modelling of grey matter volume. We establish that what seems a well-powered study may become underpowered when analyses target an age effect that is linearly separable from an age-relevant covariate such as grey matter volume. These results provide a pathway towards formal comparison and assessment of candidate markers for brain health in ageing.</p>","PeriodicalId":11640,"journal":{"name":"eLife","volume":"14 ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13657627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Large-scale prospective evaluation of co-folding across hundreds of Mac1-ligand complexes and three virtual screens.","authors":"Jongbin Kim, Galen J Correy, Brendan W Hall, Moira M Rachman, Olivier Mailhot, Takaya Togo, Ryan L Gonciarz, Priyadarshini Jaishankar, R Jeffrey Neitz, Eric R Hantz, Yagmur U Doruk, Maisie G V Stevens, Morgan E Diolaiti, Rashad Reid, Saumya Gopalkrishnan, Nevan J Krogan, Adam R Renslo, Alan Ashworth, Brian K Shoichet, James S Fraser","doi":"10.7554/eLife.110475","DOIUrl":"10.7554/eLife.110475","url":null,"abstract":"<p><p>Accurate prediction of ligand-bound protein complexes and ranking them by affinity are central problems in drug discovery. While deep-learning co-folding methods can help address these challenges, their evaluation has been hampered by the difficulties in assessing independence from training data and insufficiently large test sets. Here, we test the ability of co-folding methods to predict the structures of 551 ligands, 489 of which are of sufficient quality for evaluation, bound to the SARS-CoV-2 NSP3 macrodomain (Mac1) that were determined after the training cutoff dates. AlphaFold3 (AF3), Boltz-2, and Chai-1 each reproduced >50% of the Mac1 ligand poses to better than 2 Å root-mean-square deviation of experiment. Despite the potential for co-folding to describe protein conformational changes that stabilize ligand binding, we did not find that common conformational rearrangements, including peptide flip and a large loop opening, were recapitulated by the co-folding prediction. For AF3 and Chai-1, ligand pose prediction confidence weakly, but significantly, tracked experimental potency, while DOCK3.7 energies were only weakly correlated. Boltz-2 affinity predictions showed the strongest correlation with measured potency and, after calibration, achieved lower mean absolute error than a baseline predictor. We next assessed whether co-folding scores could rescore docking hit lists to distinguish true ligands from non-binders among hundreds of molecules prospectively experimentally tested against AmpC β-lactamase, the dopamine D4, and the σ₂ receptors. AF3 ligand pose confidence values did not separate true ligands from high-scoring false positives as effectively as docking scores or Boltz-2 affinity predictions did. Taken together, the modest, but independent correlations of docking score and co-folding confidence or affinity suggest that integrating physics-based and deep-learning approaches may help with hit prioritization and subsequent optimization in structure-based ligand discovery.</p>","PeriodicalId":11640,"journal":{"name":"eLife","volume":"15 ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13657626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A membrane-disruptive action of VBIT-4 challenges its role as a widely used VDAC1 oligomerization inhibitor.","authors":"Varun Ravishankar, Luís Borges-Araújo, Megha Rajendran, Elodie Lafargue, Deborah Byrne, Nicolas Buzhinsky, Mya S Wolfe, Wendy Fitzgerald, Nina A Bautista, Bethel G Beyene, Motahareh G Larimi, Jean-Pierre Duneau, James Sturgis, Sergey M Bezrukov, Ignacio Casuso, Tatiana K Rostovtseva, Lucie Bergdoll","doi":"10.7554/eLife.111980","DOIUrl":"10.7554/eLife.111980","url":null,"abstract":"<p><p>Voltage-dependent anion channel (VDAC) is the most abundant protein of the mitochondrial outer membrane and a key regulator of metabolite exchange and mitochondrial physiology. Its oligomerization has been proposed to control processes such as mitochondrial DNA release and membrane remodeling, yet the underlying mechanisms remain poorly defined. VBIT-4 has been widely used as a putative inhibitor of VDAC1 oligomerization, despite limited mechanistic validation. Here, using high-speed atomic force microscopy (AFM), we visualized VDAC1 assemblies in lipid membranes and examined the effect of VBIT-4. Unexpectedly, VBIT-4 induced membrane defects and permeabilization at micromolar concentrations, independently of VDAC1. Quantitative AFM analysis further shows that VBIT-4 does not alter VDAC1 cluster organization. Complementary electrophysiology, microscale thermophoresis, and coarse-grained molecular dynamics demonstrate that VBIT-4 partitions into lipid bilayers, increases membrane permeability, and destabilizes membrane structure, without detectable effects on VDAC1 channel properties or assemblies. Consistent with this mechanism, VBIT-4 induces VDAC1-independent cytotoxicity in HeLa cells at concentrations above 10 µM. Together, these results demonstrate that VBIT-4 does not act as a specific inhibitor of VDAC1 oligomerization but instead functions as a membrane-active compound. This work provides a revised framework for interpreting studies using VBIT-4 and highlights the importance of systematically assessing drug-membrane interactions when targeting membrane proteins.</p>","PeriodicalId":11640,"journal":{"name":"eLife","volume":"15 ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13652541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149147481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}