Nature Cell Biology最新文献_第4页

Chromosome mis-segregation triggers cell cycle arrest through a mechanosensitive nuclear envelope checkpoint 染色体错分离通过机械敏感的核膜检查点触发细胞周期阻滞

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2025-01-08 DOI: 10.1038/s41556-024-01565-x

Solène Hervé, Andrea Scelfo, Gabriele Bersano Marchisio, Marine Grison, Kotryna Vaidžiulytė, Marie Dumont, Annapaola Angrisani, Adib Keikhosravi, Gianluca Pegoraro, Mathieu Deygas, Guilherme P. F. Nader, Anne-Sophie Macé, Matteo Gentili, Alice Williart, Nicolas Manel, Matthieu Piel, Yekaterina A. Miroshnikova, Daniele Fachinetti

{"title":"Chromosome mis-segregation triggers cell cycle arrest through a mechanosensitive nuclear envelope checkpoint","authors":"Solène Hervé, Andrea Scelfo, Gabriele Bersano Marchisio, Marine Grison, Kotryna Vaidžiulytė, Marie Dumont, Annapaola Angrisani, Adib Keikhosravi, Gianluca Pegoraro, Mathieu Deygas, Guilherme P. F. Nader, Anne-Sophie Macé, Matteo Gentili, Alice Williart, Nicolas Manel, Matthieu Piel, Yekaterina A. Miroshnikova, Daniele Fachinetti","doi":"10.1038/s41556-024-01565-x","DOIUrl":"10.1038/s41556-024-01565-x","url":null,"abstract":"Errors during cell division lead to aneuploidy, which is associated with genomic instability and cell transformation. In response to aneuploidy, cells activate the tumour suppressor p53 to elicit a surveillance mechanism that halts proliferation and promotes senescence. The molecular sensors that trigger this checkpoint are unclear. Here, using a tunable system of chromosome mis-segregation, we show that mitotic errors trigger nuclear deformation, nuclear softening, and lamin and heterochromatin alterations, leading to rapid p53/p21 activation upon mitotic exit in response to changes in nuclear mechanics. We identify mTORC2 and ATR as nuclear deformation sensors upstream of p53/p21 activation. While triggering mitotic arrest, the chromosome mis-segregation-induced alterations of nuclear envelope mechanics provide a fitness advantage for aneuploid cells by promoting nuclear deformation resilience and enhancing pro-invasive capabilities. Collectively, this work identifies a nuclear mechanical checkpoint triggered by altered chromatin organization that probably plays a critical role in cellular transformation and cancer progression. Hervé, Scelfo et al. show that chromosome mis-segregation induces mTORC2- and ATR-mediated p53 activation through a mechanosensitive checkpoint at the nuclear envelope triggered by altered heterochromatin content and increased nuclear membrane tension.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 1","pages":"73-86"},"PeriodicalIF":17.3,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41556-024-01565-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142936063","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}

引用次数: 0

FAT1 alterations contribute to chromosomal instability in cancer cells FAT1的改变有助于癌细胞的染色体不稳定性

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2025-01-08 DOI: 10.1038/s41556-024-01559-9

引用次数: 0

Mitochondrial YME1L1 governs unoccupied protein translocase channels 线粒体YME1L1控制未占用的蛋白质转位酶通道

IF 21.3 1区生物学

Nature Cell Biology Pub Date : 2025-01-07 DOI: 10.1038/s41556-024-01571-z

Meng-Chieh Hsu, Hiroki Kinefuchi, Linlin Lei, Reika Kikuchi, Koji Yamano, Richard J. Youle

{"title":"Mitochondrial YME1L1 governs unoccupied protein translocase channels","authors":"Meng-Chieh Hsu, Hiroki Kinefuchi, Linlin Lei, Reika Kikuchi, Koji Yamano, Richard J. Youle","doi":"10.1038/s41556-024-01571-z","DOIUrl":"https://doi.org/10.1038/s41556-024-01571-z","url":null,"abstract":"Mitochondrial protein import through the outer and inner membranes is key to mitochondrial biogenesis. Recent studies have explored how cells respond when import is impaired by a variety of different insults. Here, we developed a mammalian import blocking system using dihydrofolate reductase fused to the N terminus of the inner membrane protein MIC60. While stabilization of the dihydrofolate reductase domain by methotrexate inhibited endogenous mitochondrial protein import, it neither activated the transcription factor ATF4, nor was affected by ATAD1 expression or by VCP/p97 inhibition. On the other hand, notably, plugging the channel of translocase of the outer membrane) induced YME1L1, an ATP-dependent protease, to eliminate translocase of the inner membrane (TIM23) channel components TIMM17A and TIMM23. The data suggest that unoccupied TIM23 complexes expose a C-terminal degron on TIMM17A to YME1L1 for degradation. Import plugging caused a cell growth defect and loss of YME1L1 exacerbated the growth inhibition, showing the protective effect of YME1L1 activity. YME1L1 seems to play a crucial role in mitochondrial quality control to counteract precursor stalling in the translocase of the outer membrane complex and unoccupied TIM23 channels.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"30 1","pages":""},"PeriodicalIF":21.3,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142934769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Phase separation of initiation hubs on cargo is a trigger switch for selective autophagy 起始枢纽在货物上的相分离是选择性自噬的触发开关

IF 21.3 1区生物学

Nature Cell Biology Pub Date : 2025-01-07 DOI: 10.1038/s41556-024-01572-y

Mariya Licheva, Jeremy Pflaum, Riccardo Babic, Hector Mancilla, Jana Elsässer, Emily Boyle, David M. Hollenstein, Jorge Jimenez-Niebla, Jonas Pleyer, Mio Heinrich, Franz-Georg Wieland, Joachim Brenneisen, Christopher Eickhorst, Johann Brenner, Shan Jiang, Markus Hartl, Sonja Welsch, Carola Hunte, Jens Timmer, Florian Wilfling, Claudine Kraft

{"title":"Phase separation of initiation hubs on cargo is a trigger switch for selective autophagy","authors":"Mariya Licheva, Jeremy Pflaum, Riccardo Babic, Hector Mancilla, Jana Elsässer, Emily Boyle, David M. Hollenstein, Jorge Jimenez-Niebla, Jonas Pleyer, Mio Heinrich, Franz-Georg Wieland, Joachim Brenneisen, Christopher Eickhorst, Johann Brenner, Shan Jiang, Markus Hartl, Sonja Welsch, Carola Hunte, Jens Timmer, Florian Wilfling, Claudine Kraft","doi":"10.1038/s41556-024-01572-y","DOIUrl":"https://doi.org/10.1038/s41556-024-01572-y","url":null,"abstract":"Autophagy is a key cellular quality control mechanism. Nutrient stress triggers bulk autophagy, which nonselectively degrades cytoplasmic material upon formation and liquid–liquid phase separation of the autophagy-related gene 1 (Atg1) complex. In contrast, selective autophagy eliminates protein aggregates, damaged organelles and other cargoes that are targeted by an autophagy receptor. Phase separation of cargo has been observed, but its regulation and impact on selective autophagy are poorly understood. Here, we find that key autophagy biogenesis factors phase separate into initiation hubs at cargo surfaces in yeast, subsequently maturing into sites that drive phagophore nucleation. This phase separation is dependent on multivalent, low-affinity interactions between autophagy receptors and cargo, creating a dynamic cargo surface. Notably, high-affinity interactions between autophagy receptors and cargo complexes block initiation hub formation and autophagy progression. Using these principles, we converted the mammalian reovirus nonstructural protein µNS, which accumulates as particles in the yeast cytoplasm that are not degraded, into a neo-cargo that is degraded by selective autophagy. We show that initiation hubs also form on the surface of different cargoes in human cells and are key to establish the connection to the endoplasmic reticulum, where the phagophore assembly site is formed to initiate phagophore biogenesis. Overall, our findings suggest that regulated phase separation underscores the initiation of both bulk and selective autophagy in evolutionarily diverse organisms.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"48 1","pages":""},"PeriodicalIF":21.3,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142934552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Metabolic rewiring in skin epidermis drives tolerance to oncogenic mutations 皮肤表皮的代谢重新布线驱动对致癌突变的耐受性

IF 21.3 1区生物学

Nature Cell Biology Pub Date : 2025-01-06 DOI: 10.1038/s41556-024-01574-w

Anupama Hemalatha, Zongyu Li, David G. Gonzalez, Catherine Matte-Martone, Karen Tai, Elizabeth Lathrop, Daniel Gil, Smirthy Ganesan, Lauren E. Gonzalez, Melissa Skala, Rachel J. Perry, Valentina Greco

{"title":"Metabolic rewiring in skin epidermis drives tolerance to oncogenic mutations","authors":"Anupama Hemalatha, Zongyu Li, David G. Gonzalez, Catherine Matte-Martone, Karen Tai, Elizabeth Lathrop, Daniel Gil, Smirthy Ganesan, Lauren E. Gonzalez, Melissa Skala, Rachel J. Perry, Valentina Greco","doi":"10.1038/s41556-024-01574-w","DOIUrl":"https://doi.org/10.1038/s41556-024-01574-w","url":null,"abstract":"Skin epithelial stem cells correct aberrancies induced by oncogenic mutations. Oncogenes invoke different strategies of epithelial tolerance; while wild-type cells outcompete β-catenin-gain-of-function (βcatGOF) cells, HrasG12V cells outcompete wild-type cells. Here we ask how metabolic states change as wild-type stem cells interface with mutant cells and drive different cell-competition outcomes. By tracking the endogenous redox ratio (NAD(P)H/FAD) with single-cell resolution in the same mouse over time, we discover that βcatGOF and HrasG12V mutations, when interfaced with wild-type epidermal stem cells, lead to a rapid drop in redox ratios, indicating more oxidized cellular redox. However, the resultant redox differential persists through time in βcatGOF, whereas it is flattened rapidly in the HrasG12Vmodel. Using 13C liquid chromatography–tandem mass spectrometry, we find that the βcatGOF and HrasG12V mutant epidermis increase the fractional contribution of glucose through the oxidative tricarboxylic acid cycle. Treatment with metformin, a modifier of cytosolic redox, inhibits downstream mutant phenotypes and reverses cell-competition outcomes of both mutant models.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"5 1","pages":""},"PeriodicalIF":21.3,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142929480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Chaperone-mediated insertion of mitochondrial import receptor TOM70 protects against diet-induced obesity 伴侣介导的线粒体输入受体TOM70的插入可防止饮食引起的肥胖

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2025-01-03 DOI: 10.1038/s41556-024-01555-z

Pedro Latorre-Muro, Tevis Vitale, Matthew Ravichandran, Katherine Zhang, Jonathan M. Palozzi, Christopher F. Bennett, Arantza Lamas-Paz, Jee Hyung Sohn, Thomas D. Jackson, Mark Jedrychowski, Steven P. Gygi, Shingo Kajimura, Anna Schmoker, Hyesung Jeon, Michael J. Eck, Pere Puigserver

{"title":"Chaperone-mediated insertion of mitochondrial import receptor TOM70 protects against diet-induced obesity","authors":"Pedro Latorre-Muro, Tevis Vitale, Matthew Ravichandran, Katherine Zhang, Jonathan M. Palozzi, Christopher F. Bennett, Arantza Lamas-Paz, Jee Hyung Sohn, Thomas D. Jackson, Mark Jedrychowski, Steven P. Gygi, Shingo Kajimura, Anna Schmoker, Hyesung Jeon, Michael J. Eck, Pere Puigserver","doi":"10.1038/s41556-024-01555-z","DOIUrl":"10.1038/s41556-024-01555-z","url":null,"abstract":"Outer mitochondrial membrane (OMM) proteins communicate with the cytosol and other organelles, including the endoplasmic reticulum. This communication is important in thermogenic adipocytes to increase the energy expenditure that controls body temperature and weight. However, the regulatory mechanisms of OMM protein insertion are poorly understood. Here the stress-induced cytosolic chaperone PPID (peptidyl–prolyl isomerase D/cyclophilin 40/Cyp40) drives OMM insertion of the mitochondrial import receptor TOM70 that regulates body temperature and weight in obese mice, and respiratory/thermogenic function in brown adipocytes. PPID PPIase activity and C-terminal tetratricopeptide repeats, which show specificity towards TOM70 core and C-tail domains, facilitate OMM insertion. Our results provide an unprecedented role for endoplasmic-reticulum-stress-activated chaperones in controlling energy metabolism through a selective OMM protein insertion mechanism with implications in adaptation to cold temperatures and high-calorie diets. Latorre-Muro et al. show that the cytosolic chaperone PPID drives insertion of the mitochondrial import receptor TOM70 into the mitochondrial outer membrane, thereby regulating body temperature, glucose homeostasis and body weight in obese mice.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 1","pages":"130-140"},"PeriodicalIF":17.3,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142916956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

A nucleolar mechanism suppresses organismal proteostasis by modulating TGFβ/ERK signalling 核仁机制通过调节TGFβ/ERK信号传导来抑制机体的蛋白质停滞

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2025-01-03 DOI: 10.1038/s41556-024-01564-y

Huadong Zhu, Reut Bruck-Haimson, Adam Zaretsky, Irit Cohen, Roni Falk, Hanna Achache, Yonatan B. Tzur, Ehud Cohen

{"title":"A nucleolar mechanism suppresses organismal proteostasis by modulating TGFβ/ERK signalling","authors":"Huadong Zhu, Reut Bruck-Haimson, Adam Zaretsky, Irit Cohen, Roni Falk, Hanna Achache, Yonatan B. Tzur, Ehud Cohen","doi":"10.1038/s41556-024-01564-y","DOIUrl":"10.1038/s41556-024-01564-y","url":null,"abstract":"The protein homeostasis (proteostasis) network encompasses a myriad of mechanisms that maintain the integrity of the proteome by controlling various biological functions, including protein folding and degradation. Alas, ageing-associated decline in the efficiency of this network enables protein aggregation and consequently the development of late-onset neurodegenerative disorders, such as Alzheimer’s disease. Accordingly, the maintenance of proteostasis through late stages of life bears the promise to delay the emergence of these devastating diseases. Yet the identification of proteostasis regulators is needed to assess the feasibility of this approach. Here we report that knocking down the activity of the nucleolar FIB-1–NOL-56 complex protects model nematodes from proteotoxicity of the Alzheimer’s disease-causing amyloid-β peptide and of abnormally long poly-glutamine stretches. This mechanism promotes proteostasis across tissues by modulating the activity of TGFβ signalling and by enhancing proteasome activity. Our findings point at research avenues towards the development of proteostasis-promoting therapies for neurodegenerative maladies. Zhu et al. show that disabling the nucleolar FIB-1–NOL-56 complex protects Caenorhabditis elegans from the toxicity of neurodegeneration-linked protein aggregates across tissues by modulating TGFβ signalling and enhancing proteasome activity.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 1","pages":"87-102"},"PeriodicalIF":17.3,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142916957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Speckle signatures dictate cancer prognosis 斑点特征指示癌症预后

IF 21.3 1区生物学

Nature Cell Biology Pub Date : 2025-01-03 DOI: 10.1038/s41556-024-01569-7

Hiro Takakuwa, Tetsuro Hirose

引用次数: 0

Nuclear speckles regulate functional programs in cancer 核斑点调节癌症的功能程序

IF 21.3 1区生物学

Nature Cell Biology Pub Date : 2025-01-02 DOI: 10.1038/s41556-024-01570-0

Katherine A. Alexander, Ruofan Yu, Nicolas Skuli, Nathan J. Coffey, Son Nguyen, Christine L. Faunce, Hua Huang, Ian P. Dardani, Austin L. Good, Joan Lim, Catherine Y. Li, Nicholas Biddle, Eric F. Joyce, Arjun Raj, Daniel Lee, Brian Keith, M. Celeste Simon, Shelley L. Berger

{"title":"Nuclear speckles regulate functional programs in cancer","authors":"Katherine A. Alexander, Ruofan Yu, Nicolas Skuli, Nathan J. Coffey, Son Nguyen, Christine L. Faunce, Hua Huang, Ian P. Dardani, Austin L. Good, Joan Lim, Catherine Y. Li, Nicholas Biddle, Eric F. Joyce, Arjun Raj, Daniel Lee, Brian Keith, M. Celeste Simon, Shelley L. Berger","doi":"10.1038/s41556-024-01570-0","DOIUrl":"https://doi.org/10.1038/s41556-024-01570-0","url":null,"abstract":"Nuclear speckles are dynamic nuclear bodies characterized by high concentrations of factors involved in RNA production. Although the contents of speckles suggest multifaceted roles in gene regulation, their biological functions are unclear. Here we investigate speckle variation in human cancer, finding two main signatures. One speckle signature was similar to healthy adjacent tissues, whereas the other was dissimilar, and considered an aberrant cancer speckle state. Aberrant speckles show altered positioning within the nucleus, higher levels of the TREX RNA export complex and correlate with poorer patient outcomes in clear cell renal cell carcinoma (ccRCC), a cancer typified by hyperactivation of the HIF-2α transcription factor. We demonstrate that HIF-2α promotes physical association of certain target genes with speckles depending on HIF-2α protein speckle-targeting motifs, defined in this study. We identify homologous speckle-targeting motifs within many transcription factors, suggesting that DNA-speckle targeting may be a general gene regulatory mechanism. Integrating functional, genomic and imaging studies, we show that HIF-2α gene regulatory programs are impacted by speckle state and by abrogation of HIF-2α-driven speckle targeting. These findings suggest that, in ccRCC, a key biological function of nuclear speckles is to modulate expression of select HIF-2α-regulated target genes that, in turn, influence patient outcomes. Beyond ccRCC, tumour speckle states broadly correlate with altered functional pathways and expression of speckle-associated gene neighbourhoods, exposing a general link between nuclear speckles and gene expression dysregulation in human cancer.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"68 1","pages":""},"PeriodicalIF":21.3,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

The transcription factor GABPA is a master regulator of naive pluripotency 转录因子GABPA是初始多能性的主要调控因子

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2025-01-02 DOI: 10.1038/s41556-024-01554-0

Chengjie Zhou, Meng Wang, Chunxia Zhang, Yi Zhang

{"title":"The transcription factor GABPA is a master regulator of naive pluripotency","authors":"Chengjie Zhou, Meng Wang, Chunxia Zhang, Yi Zhang","doi":"10.1038/s41556-024-01554-0","DOIUrl":"10.1038/s41556-024-01554-0","url":null,"abstract":"The establishment of naive pluripotency is a continuous process starting with the generation of inner cell mass (ICM) that then differentiates into epiblast (EPI). Recent studies have revealed key transcription factors (TFs) for ICM formation, but which TFs initiate EPI specification remains unknown. Here, using a targeted rapid protein degradation system, we show that GABPA is not only a regulator of major ZGA, but also a master EPI specifier required for naive pluripotency establishment by regulating 47% of EPI genes during E3.5 to E4.5 transition. Chromatin binding dynamics analysis suggests that GABPA controls EPI formation at least partly by binding to the ICM gene promoters occupied by the pluripotency regulators TFAP2C and SOX2 at E3.5 to establish naive pluripotency at E4.5. Our study not only uncovers GABPA as a master pluripotency regulator, but also supports the notion that mammalian pluripotency establishment requires a dynamic and stepwise multi-TF regulatory network. Zhang and colleagues identify the transcription factor GABPA as a regulator of zygotic genome activation, epiblast formation and naive pluripotency establishment.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 1","pages":"48-58"},"PeriodicalIF":17.3,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41556-024-01554-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911692","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}

引用次数: 0