Molecular Biology of the Cell最新文献_第4页

Spatial and temporal signatures of cell competition revealed by K-function analysis. K 功能分析揭示了细胞竞争的空间和时间特征。

IF 3.1 3区生物学

Molecular Biology of the Cell Pub Date : 2025-03-26 DOI: 10.1091/mbc.E24-10-0481

Nathan J Day, Jasmine Michalowska, Manasi Kelkar, Giulia Vallardi, Guillaume Charras, Alan R Lowe

{"title":"Spatial and temporal signatures of cell competition revealed by K-function analysis.","authors":"Nathan J Day, Jasmine Michalowska, Manasi Kelkar, Giulia Vallardi, Guillaume Charras, Alan R Lowe","doi":"10.1091/mbc.E24-10-0481","DOIUrl":"https://doi.org/10.1091/mbc.E24-10-0481","url":null,"abstract":"Cell competition is often categorised into mechanical competition, during which loser cell elimination is induced by long-range mechanical effects, and biochemical competition, during which loser cell elimination results from direct cell-cell contacts. Before confluence, proliferation of winner cells has often been hypothesised to gov- ern competition. Conversely, elimination of loser cells is thought to induce cell proliferation in its vicinity. However, causality is challenging to establish. To address this, we compute spatiotemporal signatures of competitive interac- tions using K-function clustering analysis. For this, we acquire long-term time lapses of two examples of mechanical (ScrKD) and biochemical (RasV12) compe- tition. We then segment cells, track them, and detect mitoses as well as elimina- tions. Finally, we perform K-function clustering to highlight spatiotemporal regions in which wild-type cell proliferation is enhanced or repressed around an elimination event. Our analysis reveals striking differences between the two types of competition. In the ScrKD competition, elimination seems driven by diffuse proliferation that does not cluster near the immediate elimination site. In contrast, RasV12 cell elimination is preceded by clustered proliferation of wild-type cells in the vicinity of the eventual RasV12 extrusion. Following loser elimination, an increase in local wild-type cell proliferation is observed in both competitions, although the timing and duration of these responses vary. This study not only sheds light on the diverse mechanisms of cell competition but also underscores the complexity of cellular interactions in tissue dynamics, providing new perspectives on cellular quality control and a new quantitative approach to characterise these interactions.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"mbcE24100481"},"PeriodicalIF":3.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HaloPROTAC3 treatment activates the unfolded protein response of the endoplasmic reticulum in non-engineered mammalian cell lines. HaloPROTAC3处理激活非工程哺乳动物细胞系内质网的未折叠蛋白反应。

IF 3.1 3区生物学

Molecular Biology of the Cell Pub Date : 2025-03-19 DOI: 10.1091/mbc.E24-08-0342

Aleksandra S Anisimova, G Elif Karagöz

引用次数: 0

Asymmetry of centrosomes in Drosophila neural stem cells requires protein phosphatase 4. 果蝇神经干细胞中心体的不对称性需要蛋白磷酸酶4。

IF 3.1 3区生物学

Molecular Biology of the Cell Pub Date : 2025-03-12 DOI: 10.1091/mbc.E25-01-0021

Roberto Carlos Segura, Emmanuel Gallaud, Adam von Barnau Sythoff, Kumar Aavula, Jennifer A Taylor, Danielle Vahdat, Fabian Otte, Jan Pielage, Clemens Cabernard

{"title":"Asymmetry of centrosomes in Drosophila neural stem cells requires protein phosphatase 4.","authors":"Roberto Carlos Segura, Emmanuel Gallaud, Adam von Barnau Sythoff, Kumar Aavula, Jennifer A Taylor, Danielle Vahdat, Fabian Otte, Jan Pielage, Clemens Cabernard","doi":"10.1091/mbc.E25-01-0021","DOIUrl":"10.1091/mbc.E25-01-0021","url":null,"abstract":"Asymmetric cell division is used by stem cells to create diverse cell types while self-renewing the stem cell population. Biased segregation of molecularly distinct centrosomes could provide a mechanism to maintain stem cell fate, induce cell differentiation or both. However, the molecular mechanisms generating molecular and functional asymmetric centrosomes remain incompletely understood. Here, we show that in asymmetrically dividing fly neural stem cells, Protein phosphatase 4 (Pp4) is necessary for correct centrosome asymmetry establishment during mitosis, and microtubule organizing center (MTOC) maintenance in interphase. Using in-vivo live cell imaging we show that while wild type neural stem cells always maintain one active MTOC, Pp4 mutant neuroblasts contain two inactive centrioles in interphase. Furthermore, centrosomes of Pp4 mutant neural stem cells mature in mitosis but fail to correctly transfer the centriolar protein Centrobin (Cnb) from the mother to the daughter centriole. Using superresolution imaging, we find that phosphomimetic Centrobin fails to accurately relocalize in mitosis. We propose that Pp4 regulates the timely relocalization of Cnb in mitosis to establish two molecularly distinct centrosomes. In addition, Pp4 is also necessary to maintain MTOC activity in interphase, ensuring biased centrosome segregation. Mechanistically, Pp4 could regulate centrosome asymmetry by dephosphorylating both Cnb and gamma-Tubulin. [Media: see text] [Media: see text] [Media: see text] [Media: see text] [Media: see text].","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"mbcE25010021"},"PeriodicalIF":3.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Adaptive protein synthesis in genetic models of copper deficiency and childhood neurodegeneration. 铜缺乏和儿童神经变性遗传模型中的适应性蛋白合成。

IF 3.1 3区生物学

Molecular Biology of the Cell Pub Date : 2025-03-01 Epub Date: 2025-01-29 DOI: 10.1091/mbc.E24-11-0512

Alicia R Lane, Noah E Scher, Shatabdi Bhattacharjee, Stephanie A Zlatic, Anne M Roberts, Avanti Gokhale, Kaela S Singleton, Duc M Duong, Mike McKenna, William L Liu, Alina Baiju, Felix G Rivera Moctezuma, Tommy Tran, Atit A Patel, Lauren B Clayton, Michael J Petris, Levi B Wood, Anupam Patgiri, Alysia D Vrailas-Mortimer, Daniel N Cox, Blaine R Roberts, Erica Werner, Victor Faundez

{"title":"Adaptive protein synthesis in genetic models of copper deficiency and childhood neurodegeneration.","authors":"Alicia R Lane, Noah E Scher, Shatabdi Bhattacharjee, Stephanie A Zlatic, Anne M Roberts, Avanti Gokhale, Kaela S Singleton, Duc M Duong, Mike McKenna, William L Liu, Alina Baiju, Felix G Rivera Moctezuma, Tommy Tran, Atit A Patel, Lauren B Clayton, Michael J Petris, Levi B Wood, Anupam Patgiri, Alysia D Vrailas-Mortimer, Daniel N Cox, Blaine R Roberts, Erica Werner, Victor Faundez","doi":"10.1091/mbc.E24-11-0512","DOIUrl":"10.1091/mbc.E24-11-0512","url":null,"abstract":"Rare inherited diseases caused by mutations in the copper transporters SLC31A1 (CTR1) or ATP7A induce copper deficiency in the brain, causing seizures and neurodegeneration in infancy through poorly understood mechanisms. Here, we used multiple model systems to characterize the molecular mechanisms by which neuronal cells respond to copper deficiency. Targeted deletion of CTR1 in neuroblastoma cells produced copper deficiency that produced a metabolic shift favoring glycolysis over oxidative phosphorylation. Proteomic and transcriptomic analysis of CTR1 knockout (KO) cells revealed simultaneous up-regulation of mTORC1 and S6K signaling and reduced PERK signaling. Patterns of gene and protein expression and pharmacogenomics show increased activation of the mTORC1-S6K pathway as a prosurvival mechanism, ultimately resulting in increased protein synthesis. Spatial transcriptomic profiling of Atp7aflx/Y :: Vil1Cre/+ mice identified up-regulated protein synthesis machinery and mTORC1-S6K pathway genes in copper-deficient Purkinje neurons in the cerebellum. Genetic epistasis experiments in Drosophila demonstrated that copper deficiency dendritic phenotypes in class IV neurons are improved or rescued by increased S6k expression or 4E-BP1 (Thor) RNAi, while epidermis phenotypes are exacerbated by Akt, S6k, or raptor RNAi. Overall, we demonstrate that increased mTORC1-S6K pathway activation and protein synthesis is an adaptive mechanism by which neuronal cells respond to copper deficiency.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"ar33"},"PeriodicalIF":3.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11974963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

When everything is a master regulator, nothing is. 当一切都是主控者时，就没有什么是主控者了。

IF 3.1 3区生物学

Molecular Biology of the Cell Pub Date : 2025-03-01 DOI: 10.1091/mbc.E24-11-0494

Robert S Krauss, Michael Kyba

引用次数: 0

Behind the scenes of cellular organization: Quantifying spatial phenotypes of puncta structures with statistical models including random fields. 细胞组织的幕后：用包括随机场在内的统计模型定量点状结构的空间表型。

IF 3.1 3区生物学

Molecular Biology of the Cell Pub Date : 2025-03-01 Epub Date: 2025-01-09 DOI: 10.1091/mbc.E24-10-0461

Kyriacos Nicolaou, Josiah B Passmore, Lukas C Kapitein, Bela M Mulder, Florian Berger

{"title":"Behind the scenes of cellular organization: Quantifying spatial phenotypes of puncta structures with statistical models including random fields.","authors":"Kyriacos Nicolaou, Josiah B Passmore, Lukas C Kapitein, Bela M Mulder, Florian Berger","doi":"10.1091/mbc.E24-10-0461","DOIUrl":"10.1091/mbc.E24-10-0461","url":null,"abstract":"The cellular interior is a spatially complex environment shaped by nontrivial stochastic and biophysical processes. Within this complexity, spatial organizational principles-also called spatial phenotypes-often emerge with functional implications. However, identifying and quantifying these phenotypes in the stochastic intracellular environment is challenging. To overcome this challenge for puncta, we discuss the use of inference of point-process models that link the density of points to other imaged structures and a random field that captures hidden processes. We apply these methods to simulated data and multiplexed immunofluorescence images of Vero E6 cells. Our analysis suggests that peroxisomes are likely to be found near the perinuclear region, overlapping with the endoplasmic reticulum, and located within a distance of 1 µm to mitochondria. Moreover, the random field captures a hidden variation of the mean density in the order of 15 µm. This length scale could provide critical information for further developing mechanistic hypotheses and models. By using spatial statistical models including random fields, we add a valuable perspective to cell biology.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"ar22"},"PeriodicalIF":3.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11974956/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Large, recursive membrane platforms are associated to Trop-1, Trop-2, and protein kinase signaling for cell growth. 大的、递归的膜平台与细胞生长的Trop-1、Trop-2和蛋白激酶信号有关。

IF 3.1 3区生物学

Molecular Biology of the Cell Pub Date : 2025-03-01 Epub Date: 2025-01-09 DOI: 10.1091/mbc.E24-06-0267

Marco Trerotola, Valeria Relli, Romina Tripaldi, Pasquale Simeone, Emanuela Guerra, Andrea Sacchetti, Martina Ceci, Ludovica Pantalone, Paolo Ciufici, Antonino Moschella, Valeria R Caiolfa, Moreno Zamai, Saverio Alberti

{"title":"Large, recursive membrane platforms are associated to Trop-1, Trop-2, and protein kinase signaling for cell growth.","authors":"Marco Trerotola, Valeria Relli, Romina Tripaldi, Pasquale Simeone, Emanuela Guerra, Andrea Sacchetti, Martina Ceci, Ludovica Pantalone, Paolo Ciufici, Antonino Moschella, Valeria R Caiolfa, Moreno Zamai, Saverio Alberti","doi":"10.1091/mbc.E24-06-0267","DOIUrl":"10.1091/mbc.E24-06-0267","url":null,"abstract":"The transmembrane glycoproteins Trop-1/EpCAM and Trop-2 independently trigger Ca2+ and kinase signals for cell growth and tumor progression. Our findings indicated that Trop-1 and Trop-2 tightly colocalize at macroscopic, ruffle-like protrusions (RLP), that elevate from the cell perimeter, and locally recur over hundreds of seconds. These previously unrecognized elevated membrane regions ≥20-µm-long, up to 1.5 µm high were revealed by Z-stack analysis and three-dimensional reconstruction of signal transducer-hosting plasma membrane regions. Trop-2 stimulates cell growth through a membrane supercomplex that comprises CD9, PKCα, ion pumps, and cytoskeletal components. Our findings indicated that the growth-driving Trop-2 supercomplex assembles at RLP. RLP behaved as sites of clustering of signal transducers, of phosphorylation/activation of growth-driving kinases, as recruitment sites of PKCα and as origin of Ca2+ signaling waves, suggesting RLP to be novel signaling platforms in living cells. RLP were induced by growth factors and disappeared upon growth factor deprivation and β-actin depolymerization, candidating RLP to be functional platforms for high-dimensional signaling for cell growth.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"ar38"},"PeriodicalIF":3.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11974968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Quantitative profiling pH heterogeneity of acidic endolysosomal compartments using fluorescence lifetime imaging microscopy. 使用荧光寿命成像显微镜定量分析酸性内溶酶体区室的pH异质性。

IF 3.1 3区生物学

Molecular Biology of the Cell Pub Date : 2025-03-01 Epub Date: 2025-01-29 DOI: 10.1091/mbc.E23-06-0220

Dinghuan Deng, Youchen Guan, Ayse Sena Mutlu, Baiping Wang, Shihong Max Gao, Hui Zheng, Meng C Wang

{"title":"Quantitative profiling pH heterogeneity of acidic endolysosomal compartments using fluorescence lifetime imaging microscopy.","authors":"Dinghuan Deng, Youchen Guan, Ayse Sena Mutlu, Baiping Wang, Shihong Max Gao, Hui Zheng, Meng C Wang","doi":"10.1091/mbc.E23-06-0220","DOIUrl":"10.1091/mbc.E23-06-0220","url":null,"abstract":"The endolysosomal system plays a crucial role in maintaining cellular homeostasis and promoting organism fitness. The pH of its acidic compartments is a crucial parameter for proper function, and it is dynamically influenced by both intracellular and environmental factors. Here, we present a method based on fluorescence lifetime imaging microscopy (FLIM) for quantitatively analyzing the pH profiles of acidic endolysosomal compartments in diverse types of primary mammalian cells and in live organism Caenorhabditis elegans. This FLIM-based method exhibits high sensitivity in resolving subtle pH differences, thereby revealing heterogeneity within a cell and across cell types. This method enables rapid measurement of pH changes in the acidic endolysosomal system in response to various environmental stimuli. Furthermore, the fast FLIM measurement of pH-sensitive dyes circumvents the need for transgenic reporters and mitigates potential confounding factors associated with varying dye concentrations or excitation light intensity. This FLIM approach offers absolute pH quantification and highlights the significance of pH heterogeneity and dynamics, offering a valuable tool for investigating lysosomal functions and their regulation in various physiological and pathological contexts.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"br8"},"PeriodicalIF":3.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11974955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Deep learning-based image classification reveals heterogeneous execution of cell death fates during viral infection. 基于深度学习的图像分类揭示了病毒感染期间细胞死亡命运的异质执行。

IF 3.1 3区生物学

Molecular Biology of the Cell Pub Date : 2025-03-01 Epub Date: 2025-01-22 DOI: 10.1091/mbc.E24-10-0438

Edoardo Centofanti, Alon Oyler-Yaniv, Jennifer Oyler-Yaniv

{"title":"Deep learning-based image classification reveals heterogeneous execution of cell death fates during viral infection.","authors":"Edoardo Centofanti, Alon Oyler-Yaniv, Jennifer Oyler-Yaniv","doi":"10.1091/mbc.E24-10-0438","DOIUrl":"10.1091/mbc.E24-10-0438","url":null,"abstract":"Cell fate decisions, such as proliferation, differentiation, and death, are driven by complex molecular interactions and signaling cascades. While significant progress has been made in understanding the molecular determinants of these processes, historically, cell fate transitions were identified through light microscopy that focused on changes in cell morphology and function. Modern techniques have shifted toward probing molecular effectors to quantify these transitions, offering more precise quantification and mechanistic understanding. However, challenges remain in cases where the molecular signals are ambiguous, complicating the assignment of cell fate. During viral infection, programmed cell death (PCD) pathways, including apoptosis, necroptosis, and pyroptosis, exhibit complex signaling and molecular cross-talk. This can lead to simultaneous activation of multiple PCD pathways, which confounds assignment of cell fate based on molecular information alone. To address this challenge, we employed deep learning-based image classification of dying cells to analyze PCD in single herpes simplex virus-1 (HSV-1)-infected cells. Our approach reveals that despite heterogeneous activation of signaling, individual cells adopt predominantly prototypical death morphologies. Nevertheless, PCD is executed heterogeneously within a uniform population of virus-infected cells and varies over time. These findings demonstrate that image-based phenotyping can provide valuable insights into cell fate decisions, complementing molecular assays.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"ar29"},"PeriodicalIF":3.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11974948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tetraspanins 10 and 15 support Venezuelan equine encephalitis virus replication in astrocytoma cells. 四蛋白10和15支持委内瑞拉马脑炎病毒在星形细胞瘤细胞中的复制。

IF 3.1 3区生物学

Molecular Biology of the Cell Pub Date : 2025-03-01 Epub Date: 2025-01-29 DOI: 10.1091/mbc.E24-12-0574

Mara Duven, Alina Friedrichs, Michael G Tomlinson, Imke Steffen, Gisa Gerold

{"title":"Tetraspanins 10 and 15 support Venezuelan equine encephalitis virus replication in astrocytoma cells.","authors":"Mara Duven, Alina Friedrichs, Michael G Tomlinson, Imke Steffen, Gisa Gerold","doi":"10.1091/mbc.E24-12-0574","DOIUrl":"10.1091/mbc.E24-12-0574","url":null,"abstract":"Tetraspanins (Tspans) are transmembrane proteins that coordinate life cycle steps of viruses from distinct families. Here, we identify the human Tspan10 and Tspan15, both members of the TspanC8 subfamily, as replication factors for alphavirus Venezuelan equine encephalitis virus (VEEV) in astrocytoma cells. Pharmacological inhibition and small interfering RNA (siRNA)-mediated silencing of TspanC8 interactor a disintegrin and metalloproteinase 10 (ADAM10) reduced VEEV infection. Silencing of Tspan10, Tspan15, and ADAM10 did not affect VEEV entry but diminished viral genome replication. We report that Tspan10 is important for VEEV infection of several cell lines, while silencing of Tspan15 diminishes infection with several alphaviruses, but not flaviviruses, in astrocytoma cells. Conversely, we demonstrate that siRNA-mediated silencing of Tspan14, another member of the TspanC8 family, enhances infection with lentiviral pseudoparticles harbouring the envelope proteins of VEEV, identifying it as a restriction factor for VEEV entry. Silencing of ADAM10/Tspan15 substrate neuronal (N)-cadherin reduced VEEV infectivity, suggesting potential roles of ADAM10 substrates in VEEV infection. In sum, our study identifies three TspanC8s and ADAM10 as important modulators of VEEV infectivity.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"ar35"},"PeriodicalIF":3.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11974957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0