PLoS Biology最新文献

{"title":"Inhibition of ribosome biogenesis in the epidermis is sufficient to trigger organism-wide growth quiescence independently of nutritional status in C. elegans.","authors":"Qiuxia Zhao,&nbsp;Rekha Rangan,&nbsp;Shinuo Weng,&nbsp;Cem Özdemir,&nbsp;Elif Sarinay Cenik","doi":"10.1371/journal.pbio.3002276","DOIUrl":"10.1371/journal.pbio.3002276","url":null,"abstract":"<p><p>Interorgan communication is crucial for multicellular organismal growth, development, and homeostasis. Cell nonautonomous inhibitory cues, which limit tissue-specific growth alterations, are not well characterized due to cell ablation approach limitations. In this study, we employed the auxin-inducible degradation system in C. elegans to temporally and spatially modulate ribosome biogenesis, through depletion of essential factors (RPOA-2, GRWD-1, or TSR-2). Our findings reveal that embryo-wide inhibition of ribosome biogenesis induces a reversible early larval growth quiescence, distinguished by a unique gene expression signature that is different from starvation or dauer stages. When ribosome biogenesis is inhibited in volumetrically similar tissues, including body wall muscle, epidermis, pharynx, intestine, or germ line, it results in proportionally stunted growth across the organism to different degrees. We show that specifically inhibiting ribosome biogenesis in the epidermis is sufficient to trigger an organism-wide growth quiescence. Epidermis-specific ribosome depletion leads to larval growth quiescence at the L3 stage, reduces organism-wide protein synthesis, and induced cell nonautonomous gene expression alterations. Further molecular analysis reveals overexpression of secreted proteins, suggesting an organism-wide regulatory mechanism. We find that UNC-31, a dense-core vesicle (DCV) pathway component, plays a significant role in epidermal ribosome biogenesis-mediated growth quiescence. Our tissue-specific knockdown experiments reveal that the organism-wide growth quiescence induced by epidermal-specific ribosome biogenesis inhibition is suppressed by reducing unc-31 expression in the epidermis, but not in neurons or body wall muscles. Similarly, IDA-1, a membrane-associated protein of the DCV, is overexpressed, and its knockdown in epidermis suppresses the organism-wide growth quiescence in response to epidermal ribosome biogenesis inhibition. Finally, we observe an overall increase in DCV puncta labeled by IDA-1 when epidermal ribosome biogenesis is inhibited, and these puncta are present in or near epidermal cells. In conclusion, these findings suggest a novel mechanism of nutrition-independent multicellular growth coordination initiated from the epidermis tissue upon ribosome biogenesis inhibition.</p>","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":"21 8","pages":"e3002276"},"PeriodicalIF":9.8,"publicationDate":"2023-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10499265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10292992","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":"Rapid structural remodeling of peripheral taste neurons is independent of taste cell turnover.","authors":"Zachary D Whiddon,&nbsp;Jaleia B Marshall,&nbsp;David C Alston,&nbsp;Aaron W McGee,&nbsp;Robin F Krimm","doi":"10.1371/journal.pbio.3002271","DOIUrl":"10.1371/journal.pbio.3002271","url":null,"abstract":"<p><p>Taste bud cells are constantly replaced in taste buds as old cells die and new cells migrate into the bud. The perception of taste relies on new taste bud cells integrating with existing neural circuitry, yet how these new cells connect with a taste ganglion neuron is unknown. Do taste ganglion neurons remodel to accommodate taste bud cell renewal? If so, how much of the structure of taste axons is fixed and how much remodels? Here, we measured the motility and branching of individual taste arbors (the portion of the axon innervating taste buds) in mice over time with two-photon in vivo microscopy. Terminal branches of taste arbors continuously and rapidly remodel within the taste bud. This remodeling is faster than predicted by taste bud cell renewal, with terminal branches added and lost concurrently. Surprisingly, blocking entry of new taste bud cells with chemotherapeutic agents revealed that remodeling of the terminal branches on taste arbors does not rely on the renewal of taste bud cells. Although terminal branch remodeling was fast and intrinsically controlled, no new arbors were added to taste buds, and few were lost over 100 days. Taste ganglion neurons maintain a stable number of arbors that are each capable of high-speed remodeling. We propose that terminal branch plasticity permits arbors to locate new taste bud cells, while stability of arbor number supports constancy in the degree of connectivity and function for each neuron over time.</p>","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":"21 8","pages":"e3002271"},"PeriodicalIF":9.8,"publicationDate":"2023-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10499261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10604259","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":"An interactive deep learning-based approach reveals mitochondrial cristae topologies.","authors":"Shogo Suga,&nbsp;Koki Nakamura,&nbsp;Yu Nakanishi,&nbsp;Bruno M Humbel,&nbsp;Hiroki Kawai,&nbsp;Yusuke Hirabayashi","doi":"10.1371/journal.pbio.3002246","DOIUrl":"10.1371/journal.pbio.3002246","url":null,"abstract":"<p><p>The convolution of membranes called cristae is a critical structural and functional feature of mitochondria. Crista structure is highly diverse between different cell types, reflecting their role in metabolic adaptation. However, their precise three-dimensional (3D) arrangement requires volumetric analysis of serial electron microscopy and has therefore been limiting for unbiased quantitative assessment. Here, we developed a novel, publicly available, deep learning (DL)-based image analysis platform called Python-based human-in-the-loop workflow (PHILOW) implemented with a human-in-the-loop (HITL) algorithm. Analysis of dense, large, and isotropic volumes of focused ion beam-scanning electron microscopy (FIB-SEM) using PHILOW reveals the complex 3D nanostructure of both inner and outer mitochondrial membranes and provides deep, quantitative, structural features of cristae in a large number of individual mitochondria. This nanometer-scale analysis in micrometer-scale cellular contexts uncovers fundamental parameters of cristae, such as total surface area, orientation, tubular/lamellar cristae ratio, and crista junction density in individual mitochondria. Unbiased clustering analysis of our structural data unraveled a new function for the dynamin-related GTPase Optic Atrophy 1 (OPA1) in regulating the balance between lamellar versus tubular cristae subdomains.</p>","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":"21 8","pages":"e3002246"},"PeriodicalIF":9.8,"publicationDate":"2023-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10470929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10153179","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":"The microbiota conditions a gut milieu that selects for wild-type Salmonella Typhimurium virulence.","authors":"Ersin Gül,&nbsp;Erik Bakkeren,&nbsp;Guillem Salazar,&nbsp;Yves Steiger,&nbsp;Andrew Abi Younes,&nbsp;Melanie Clerc,&nbsp;Philipp Christen,&nbsp;Stefan A Fattinger,&nbsp;Bidong D Nguyen,&nbsp;Patrick Kiefer,&nbsp;Emma Slack,&nbsp;Martin Ackermann,&nbsp;Julia A Vorholt,&nbsp;Shinichi Sunagawa,&nbsp;Médéric Diard,&nbsp;Wolf-Dietrich Hardt","doi":"10.1371/journal.pbio.3002253","DOIUrl":"10.1371/journal.pbio.3002253","url":null,"abstract":"<p><p>Salmonella Typhimurium elicits gut inflammation by the costly expression of HilD-controlled virulence factors. This inflammation alleviates colonization resistance (CR) mediated by the microbiota and thereby promotes pathogen blooms. However, the inflamed gut-milieu can also select for hilD mutants, which cannot elicit or maintain inflammation, therefore causing a loss of the pathogen's virulence. This raises the question of which conditions support the maintenance of virulence in S. Typhimurium. Indeed, it remains unclear why the wild-type hilD allele is dominant among natural isolates. Here, we show that microbiota transfer from uninfected or recovered hosts leads to rapid clearance of hilD mutants that feature attenuated virulence, and thereby contributes to the preservation of the virulent S. Typhimurium genotype. Using mouse models featuring a range of microbiota compositions and antibiotic- or inflammation-inflicted microbiota disruptions, we found that irreversible disruption of the microbiota leads to the accumulation of hilD mutants. In contrast, in models with a transient microbiota disruption, selection for hilD mutants was prevented by the regrowing microbiota community dominated by Lachnospirales and Oscillospirales. Strikingly, even after an irreversible microbiota disruption, microbiota transfer from uninfected donors prevented the rise of hilD mutants. Our results establish that robust S. Typhimurium gut colonization hinges on optimizing its manipulation of the host: A transient and tempered microbiota perturbation is favorable for the pathogen to both flourish in the inflamed gut and also minimize loss of virulence. Moreover, besides conferring CR, the microbiota may have the additional consequence of maintaining costly enteropathogen virulence mechanisms.</p>","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":"21 8","pages":"e3002253"},"PeriodicalIF":9.8,"publicationDate":"2023-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10499267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10587087","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":"TOR complex 1 negatively regulates NDR kinase Cbk1 to control cell separation in budding yeast.","authors":"Magdalena Foltman,&nbsp;Iván Mendez,&nbsp;Joan J Bech-Serra,&nbsp;Carolina de la Torre,&nbsp;Jennifer L Brace,&nbsp;Eric L Weiss,&nbsp;María Lucas,&nbsp;Ethel Queralt,&nbsp;Alberto Sanchez-Diaz","doi":"10.1371/journal.pbio.3002263","DOIUrl":"10.1371/journal.pbio.3002263","url":null,"abstract":"<p><p>The target of rapamycin (TOR) signalling pathway plays a key role in the coordination between cellular growth and the cell cycle machinery in eukaryotes. The underlying molecular mechanisms by which TOR might regulate events after anaphase remain unknown. We show for the first time that one of the 2 TOR complexes in budding yeast, TORC1, blocks the separation of cells following cytokinesis by phosphorylation of a member of the NDR (nuclear Dbf2-related) protein-kinase family, the protein Cbk1. We observe that TORC1 alters the phosphorylation pattern of Cbk1 and we identify a residue within Cbk1 activation loop, T574, for which a phosphomimetic substitution makes Cbk1 catalytically inactive and, indeed, reproduces TORC1 control over cell separation. In addition, we identify the exocyst component Sec3 as a key substrate of Cbk1, since Sec3 activates the SNARE complex to promote membrane fusion. TORC1 activity ultimately compromises the interaction between Sec3 and a t-SNARE component. Our data indicate that TORC1 negatively regulates cell separation in budding yeast by participating in Cbk1 phosphorylation, which in turn controls the fusion of secretory vesicles transporting hydrolase at the site of division.</p>","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":"21 8","pages":"e3002263"},"PeriodicalIF":9.8,"publicationDate":"2023-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10468069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10149776","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":"In vivo recording of suprachiasmatic nucleus dynamics reveals a dominant role of arginine vasopressin neurons in circadian pacesetting.","authors":"Yusuke Tsuno,&nbsp;Yubo Peng,&nbsp;Shin-Ichi Horike,&nbsp;Mohan Wang,&nbsp;Ayako Matsui,&nbsp;Kanato Yamagata,&nbsp;Mizuki Sugiyama,&nbsp;Takahiro J Nakamura,&nbsp;Takiko Daikoku,&nbsp;Takashi Maejima,&nbsp;Michihiro Mieda","doi":"10.1371/journal.pbio.3002281","DOIUrl":"10.1371/journal.pbio.3002281","url":null,"abstract":"<p><p>The central circadian clock of the suprachiasmatic nucleus (SCN) is a network consisting of various types of neurons and glial cells. Individual cells have the autonomous molecular machinery of a cellular clock, but their intrinsic periods vary considerably. Here, we show that arginine vasopressin (AVP) neurons set the ensemble period of the SCN network in vivo to control the circadian behavior rhythm. Artificial lengthening of cellular periods by deleting casein kinase 1 delta (CK1δ) in the whole SCN lengthened the free-running period of behavior rhythm to an extent similar to CK1δ deletion specific to AVP neurons. However, in SCN slices, PER2::LUC reporter rhythms of these mice only partially and transiently recapitulated the period lengthening, showing a dissociation between the SCN shell and core with a period instability in the shell. In contrast, in vivo calcium rhythms of both AVP and vasoactive intestinal peptide (VIP) neurons in the SCN of freely moving mice demonstrated stably lengthened periods similar to the behavioral rhythm upon AVP neuron-specific CK1δ deletion, without changing the phase relationships between each other. Furthermore, optogenetic activation of AVP neurons acutely induced calcium increase in VIP neurons in vivo. These results indicate that AVP neurons regulate other SCN neurons, such as VIP neurons, in vivo and thus act as a primary determinant of the SCN ensemble period.</p>","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":"21 8","pages":"e3002281"},"PeriodicalIF":9.8,"publicationDate":"2023-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10465001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10493504","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":"Senescence in yeast is associated with amplified linear fragments of chromosome XII rather than ribosomal DNA circle accumulation.","authors":"Andre Zylstra,&nbsp;Hanane Hadj-Moussa,&nbsp;Dorottya Horkai,&nbsp;Alex J Whale,&nbsp;Baptiste Piguet,&nbsp;Jonathan Houseley","doi":"10.1371/journal.pbio.3002250","DOIUrl":"10.1371/journal.pbio.3002250","url":null,"abstract":"<p><p>The massive accumulation of extrachromosomal ribosomal DNA circles (ERCs) in yeast mother cells has been long cited as the primary driver of replicative ageing. ERCs arise through ribosomal DNA (rDNA) recombination, and a wealth of genetic data connects rDNA instability events giving rise to ERCs with shortened life span and other ageing pathologies. However, we understand little about the molecular effects of ERC accumulation. Here, we studied ageing in the presence and absence of ERCs, and unexpectedly found no evidence of gene expression differences that might indicate stress responses or metabolic feedback caused by ERCs. Neither did we observe any global change in the widespread disruption of gene expression that accompanies yeast ageing, altogether suggesting that ERCs are largely inert. Much of the differential gene expression that accompanies ageing in yeast was actually associated with markers of the senescence entry point (SEP), showing that senescence, rather than age, underlies these changes. Cells passed the SEP irrespective of ERCs, but we found the SEP to be associated with copy number amplification of a region of chromosome XII between the rDNA and the telomere (ChrXIIr) forming linear fragments up to approximately 1.8 Mb size, which arise in aged cells due to rDNA instability but through a different mechanism to ERCs. Therefore, although rDNA copy number increases dramatically with age due to ERC accumulation, our findings implicate ChrXIIr, rather than ERCs, as the primary driver of senescence during budding yeast ageing.</p>","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":"21 8","pages":"e3002250"},"PeriodicalIF":9.8,"publicationDate":"2023-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10464983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10117734","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":"Dietary change without caloric restriction maintains a youthful profile in ageing yeast.","authors":"Dorottya Horkai,&nbsp;Hanane Hadj-Moussa,&nbsp;Alex J Whale,&nbsp;Jonathan Houseley","doi":"10.1371/journal.pbio.3002245","DOIUrl":"10.1371/journal.pbio.3002245","url":null,"abstract":"<p><p>Caloric restriction increases lifespan and improves ageing health, but it is unknown whether these outcomes can be separated or achieved through less severe interventions. Here, we show that an unrestricted galactose diet in early life minimises change during replicative ageing in budding yeast, irrespective of diet later in life. Average mother cell division rate is comparable between glucose and galactose diets, and lifespan is shorter on galactose, but markers of senescence and the progressive dysregulation of gene expression observed on glucose are minimal on galactose, showing that these are not intrinsic aspects of replicative ageing but rather associated processes. Respiration on galactose is critical for minimising hallmarks of ageing, and forced respiration during ageing on glucose by overexpression of the mitochondrial biogenesis factor Hap4 also has the same effect though only in a fraction of cells. This fraction maintains Hap4 activity to advanced age with low senescence and a youthful gene expression profile, whereas other cells in the same population lose Hap4 activity, undergo dramatic dysregulation of gene expression and accumulate fragments of chromosome XII (ChrXIIr), which are tightly associated with senescence. Our findings support the existence of two separable ageing trajectories in yeast. We propose that a complete shift to the healthy ageing mode can be achieved in wild-type cells through dietary change in early life without caloric restriction.</p>","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":"21 8","pages":"e3002245"},"PeriodicalIF":9.8,"publicationDate":"2023-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10464975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10124945","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":"Relationship between journal impact factor and the thoroughness and helpfulness of peer reviews.","authors":"Anna Severin,&nbsp;Michaela Strinzel,&nbsp;Matthias Egger,&nbsp;Tiago Barros,&nbsp;Alexander Sokolov,&nbsp;Julia Vilstrup Mouatt,&nbsp;Stefan Müller","doi":"10.1371/journal.pbio.3002238","DOIUrl":"10.1371/journal.pbio.3002238","url":null,"abstract":"<p><p>The Journal Impact Factor is often used as a proxy measure for journal quality, but the empirical evidence is scarce. In particular, it is unclear how peer review characteristics for a journal relate to its impact factor. We analysed 10,000 peer review reports submitted to 1,644 biomedical journals with impact factors ranging from 0.21 to 74.7. Two researchers hand-coded sentences using categories of content related to the thoroughness of the review (Materials and Methods, Presentation and Reporting, Results and Discussion, Importance and Relevance) and helpfulness (Suggestion and Solution, Examples, Praise, Criticism). We fine-tuned and validated transformer machine learning language models to classify sentences. We then examined the association between the number and percentage of sentences addressing different content categories and 10 groups defined by the Journal Impact Factor. The median length of reviews increased with higher impact factor, from 185 words (group 1) to 387 words (group 10). The percentage of sentences addressing Materials and Methods was greater in the highest Journal Impact Factor journals than in the lowest Journal Impact Factor group. The results for Presentation and Reporting went in the opposite direction, with the highest Journal Impact Factor journals giving less emphasis to such content. For helpfulness, reviews for higher impact factor journals devoted relatively less attention to Suggestion and Solution than lower impact factor journals. In conclusion, peer review in journals with higher impact factors tends to be more thorough, particularly in addressing study methods while giving relatively less emphasis to presentation or suggesting solutions. Differences were modest and variability high, indicating that the Journal Impact Factor is a bad predictor of the quality of peer review of an individual manuscript.</p>","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":"21 8","pages":"e3002238"},"PeriodicalIF":9.8,"publicationDate":"2023-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10464996/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10251476","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":"To avoid carbon degradation in tropical forests, conserve wildlife.","authors":"Elizabeth L Bennett,&nbsp;John G Robinson","doi":"10.1371/journal.pbio.3002262","DOIUrl":"10.1371/journal.pbio.3002262","url":null,"abstract":"<p><p>Loss of large-bodied wildlife, typically from hunting, degrades the ecological processes in tropical forests that sequester and store carbon. Carbon-based markets that incentivize wildlife conservation can generate revenues to support necessary forest and hunting management.</p>","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":"21 8","pages":"e3002262"},"PeriodicalIF":9.8,"publicationDate":"2023-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10464947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10493500","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}