Journal of cell science最新文献

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Pharmacological inhibition of MCL-1 disrupts mitochondrial cristae and depletes the human neural progenitor cell pool. MCL-1的药物抑制破坏线粒体嵴并耗尽人类神经祖细胞池。
IF 3.9 3区 生物学
Journal of cell science Pub Date : 2026-10-01 Epub Date: 2026-10-15 DOI: 10.1242/jcs.265172
Marina R Hanna, James Costanzo, Madison Yarbrough, Melanie Gil, Matthew Murrow, Vivian Gama
{"title":"Pharmacological inhibition of MCL-1 disrupts mitochondrial cristae and depletes the human neural progenitor cell pool.","authors":"Marina R Hanna, James Costanzo, Madison Yarbrough, Melanie Gil, Matthew Murrow, Vivian Gama","doi":"10.1242/jcs.265172","DOIUrl":"10.1242/jcs.265172","url":null,"abstract":"<p><p>Myeloid cell leukemia 1 (MCL-1) is a canonical anti-apoptotic protein crucial for early neurodevelopment. Loss of MCL-1 results in embryonic-lethal neurodevelopmental defects that cannot be rescued by other anti-apoptotic proteins of the B cell lymphoma 2 (BCL-2) family. Here, we pharmacologically inhibit MCL-1 in human neural progenitor cells and find non-apoptotic roles for MCL-1 in sustaining mitochondrial cristae integrity, fatty acid oxidation and neural progenitor identity. MCL-1 inhibition disrupts mitochondrial ultrastructure, leading to a swollen network with disorganized cristae and destabilized OPA1-MICOS machinery that fails to maintain inner mitochondrial membrane architecture. These structural defects are accompanied by displacement of ACSL1 from the outer mitochondrial membrane, impaired fatty acid oxidation, lipid droplet accumulation and reduced mitochondrial oxygen consumption, revealing a tight link between cristae architecture and metabolic competence. Mechanistically, MCL-1 acts through two coordinated functions: maintaining cristae integrity at the inner mitochondrial membrane and retaining ACSL1 at the outer mitochondrial membrane, both independently of caspase activation. Functionally, MCL-1 inhibition selectively depletes intermediate progenitor cells without affecting proliferation, indicating a direct role in lineage progression. Together, our findings position MCL-1 upstream of OPA1, MICOS and ACSL1, and identify it as a critical coordinator of cristae organization, lipid metabolism and neural progenitor fate. This establishes mitochondrial inner membrane architecture as an instructive determinant of human neurogenesis and highlights non-canonical MCL-1 functions as critical regulators of human brain development.</p>","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":"139 19","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149182057","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
Live dynamics of induced cell-cell fusion between mitotic and interphasic cells. 有丝分裂细胞和间期细胞间诱导细胞融合的活动力学。
IF 3.9 3区 生物学
Journal of cell science Pub Date : 2026-10-01 Epub Date: 2026-10-13 DOI: 10.1242/jcs.264827
Olga Afonso, Daniel Feliciano, Jennifer Lippincott-Schwartz
{"title":"Live dynamics of induced cell-cell fusion between mitotic and interphasic cells.","authors":"Olga Afonso, Daniel Feliciano, Jennifer Lippincott-Schwartz","doi":"10.1242/jcs.264827","DOIUrl":"10.1242/jcs.264827","url":null,"abstract":"<p><p>The cell cycle is tightly regulated by checkpoint mechanisms that ensure faithful duplication and segregation of the genome. Here, we have induced cell-cell fusion between mitotic and interphase cells to study how nuclei from different cell cycle stages behave in a shared cytoplasm. We found that mitosis is a dominant cell cycle state: the mitotic cytoplasm can drive interphase nuclei into mitosis, whereas only at high ratios of interphase versus mitotic nuclei are mitotic nuclei forced to exit mitosis. Both outcomes represent checkpoint override events with impactful consequences. Interphase nuclei forced into mitosis form aberrant mitotic spindles, show partially condensed DNA and ultimately undergo mitotic catastrophe. Conversely, forced mitotic exit results in reformation of nuclear envelope membranes around condensed chromosomes, forming nuclei with a defective nuclear import machinery. Altogether, cell-cell fusion reveals the consequences of checkpoint override, forcing nuclei through untimely cell cycle transitions, and highlights how cell-cell fusion experiments can be a powerful system for studying how competing cytoplasmic states are integrated in a shared cytoplasm, such as in muscle, placenta formation and cancer.</p>","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148919463","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
Memory of growth promotes early Ras GTPase activation to establish dominance of inherited cell ends in Schizosaccharomyces pombe. 生长记忆促进早期Ras GTPase激活,以建立遗传细胞末端的优势。
IF 3.9 3区 生物学
Journal of cell science Pub Date : 2026-10-01 Epub Date: 2026-10-12 DOI: 10.1242/jcs.264600
Walker H Vickers, Maitreyi E Das
{"title":"Memory of growth promotes early Ras GTPase activation to establish dominance of inherited cell ends in Schizosaccharomyces pombe.","authors":"Walker H Vickers, Maitreyi E Das","doi":"10.1242/jcs.264600","DOIUrl":"10.1242/jcs.264600","url":null,"abstract":"<p><p>Many eukaryotic cells maintain their polarity pattern and shape across multiple rounds of division. This requires that the daughter cells re-establish polarity at the correct site after cell division. Fission yeast cells (Schizosaccharomyces pombe) are bipolar; however, after division, growth initiates first at the old end of the cell that was inherited from the mother. This old-end dominance is dependent on that end having grown in the previous generation, suggesting that cells must recognize when an end has a history of growth. We find that this memory of growth is imparted by the growth-dependent localization of Rax1 (encoded by SPAC23G3.05c) and Rax2 proteins. Rax1 and Rax2 promote early activation of Ras1 GTPase at dividing cell ends by recruitment of its guanine nucleotide exchange factor Efc25. This enables timely transition of Cdc42 activity from the division site to the old end, thus giving this end an advantage in polarized growth. Consistently, modulating Ras1 activation via disruption of its regulators Efc25 and Gap1 leads to corresponding changes in old-end dominance. Here, we demonstrate the importance of memory of growth in maintaining persistent sites of growth from one generation to the next.</p>","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148880562","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
Rxiv-Maker - an automated template engine for streamlined scientific publications. Rxiv-Maker:用于简化科学出版物的自动模板引擎。
IF 3.9 3区 生物学
Journal of cell science Pub Date : 2026-10-01 Epub Date: 2026-10-12 DOI: 10.1242/jcs.265183
Bruno M Saraiva, Rita Carlota, António D Brito, Iván Hidalgo-Cenalmor, Guillaume Jacquemet, Ricardo Henriques
{"title":"Rxiv-Maker - an automated template engine for streamlined scientific publications.","authors":"Bruno M Saraiva, Rita Carlota, António D Brito, Iván Hidalgo-Cenalmor, Guillaume Jacquemet, Ricardo Henriques","doi":"10.1242/jcs.265183","DOIUrl":"10.1242/jcs.265183","url":null,"abstract":"<p><p>Preprints have transformed how biologists share results; yet, how well a preprint reads still depends on formatting, a task that has shifted from publishers to authors. Cell biology has also become increasingly quantitative, with conclusions resting on multi-step image analysis, for which figures, values and statistics are revised repeatedly across a project. Keeping a well-formatted manuscript in step with the latest analysis is tedious and error prone. We introduce Rxiv-Maker, an open-source framework that lets authors write in simple Markdown and produce a formatted article, as a PDF or an editable Word document, with consistent styling, automatic figure and citation numbering, and reliable cross-referencing. For quantitative work, it can optionally regenerate figures and recompute reported values directly from the data, so the text stays consistent with the analysis. Built on familiar tools such as Git and Visual Studio Code, it gives a transparent, collaborative path from analysis to a submission-ready preprint. Researchers have already used Rxiv-Maker for cell biology studies spanning bacterial cell cycle analysis, filopodia proteomics and zebrafish live imaging, showing that it supports reproducible reporting of genuine biological findings.</p>","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891710","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
Lamin B1 coordinates the assembly of the nuclear lamina. 层蛋白B1协调核层的组装。
IF 3.9 3区 生物学
Journal of cell science Pub Date : 2026-10-01 Epub Date: 2026-10-15 DOI: 10.1242/jcs.265156
JoonYoung R Kim, Paul H Kim, Yiping Tu, James Carroll, Jenna P Koerner, Stephen G Young, Loren G Fong
{"title":"Lamin B1 coordinates the assembly of the nuclear lamina.","authors":"JoonYoung R Kim, Paul H Kim, Yiping Tu, James Carroll, Jenna P Koerner, Stephen G Young, Loren G Fong","doi":"10.1242/jcs.265156","DOIUrl":"10.1242/jcs.265156","url":null,"abstract":"<p><p>The nuclear lamina provides essential mechanical stability to protect the genome; yet, how lamins target the nuclear rim and assemble into an organized meshwork remains unclear. To address this, we generated smooth muscle cells lacking all three lamin genes (Lmna, Lmnb1 and Lmnb2; 'LKO cells') and expressed individual lamins at physiological levels. All lamins localized to the nuclear rim but with distinct requirements: lamin B1 and lamin B2 required farnesylation, whereas prelamin A did not. Lamin C and mature lamin A also localized efficiently, demonstrating that C-terminal processing is not required for A-type lamin targeting. Despite correct targeting, lamins differed in their ability to form organized meshworks. Lamin B1 alone generated a normal fibrillar network, whereas lamin A, lamin C and lamin B2 formed disorganized structures with large gaps. Co-expression of lamin A and lamin C did not rescue this defect. In contrast, co-expression with lamin B1 restored proper meshwork organization for all lamins and was essential for nuclear lamina assembly during cell division. These findings identify lamin B1 as the central organizer of nuclear lamina architecture.</p>","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038924","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
Correction: Outer kinetochore proteins form linear elements to regulate vesicle transport. 更正:外着丝点蛋白形成线性元件来调节囊泡运输。
IF 3.9 3区 生物学
Journal of cell science Pub Date : 2026-10-01 Epub Date: 2026-10-16 DOI: 10.1242/jcs.265311
Shane J Kowaleski, Alexis Bridgewater, Cody Saraceno, Miranda Dudek, Federico Pelisch, Joshua N Bembenek
{"title":"Correction: Outer kinetochore proteins form linear elements to regulate vesicle transport.","authors":"Shane J Kowaleski, Alexis Bridgewater, Cody Saraceno, Miranda Dudek, Federico Pelisch, Joshua N Bembenek","doi":"10.1242/jcs.265311","DOIUrl":"https://doi.org/10.1242/jcs.265311","url":null,"abstract":"","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":"139 19","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149194030","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
In situ visualization of autophagy reveals the presence of vesicles at the expanding phagophore rim. 自噬的原位可视化显示在扩大的吞噬细胞边缘存在囊泡。
IF 3.9 3区 生物学
Journal of cell science Pub Date : 2026-09-24 DOI: 10.1242/jcs.265302
Claire Ortmann de Percin Northumberland, Mariya Licheva, Rahel Dabrowski, Rubén Gómez-Sánchez, Sabrina Berkamp, Philipp Schönnenbeck, Martin Graef, Claudine Kraft, Carsten Sachse
{"title":"In situ visualization of autophagy reveals the presence of vesicles at the expanding phagophore rim.","authors":"Claire Ortmann de Percin Northumberland, Mariya Licheva, Rahel Dabrowski, Rubén Gómez-Sánchez, Sabrina Berkamp, Philipp Schönnenbeck, Martin Graef, Claudine Kraft, Carsten Sachse","doi":"10.1242/jcs.265302","DOIUrl":"https://doi.org/10.1242/jcs.265302","url":null,"abstract":"<p><p>The autophagy core machinery mediates the enclosure of cytosolic cargo destined for degradation in the lysosome. The Atg9-Atg2-Atg18 complex coordinates phagophore expansion via directed lipid transfer until closure of the phagophore rim. Using an Atg2 variant (Atg2-PM4) as a model of decelerated autophagosome biogenesis, we visualized the morphological states prior to autophagosome closure by cryogenic correlative light and electron microscopy in S. cerevisiae. Using in situ cryo-electron tomography, we find an enlarged rim morphology of an expanding phagophore in Atg2-PM4 cells in comparison with Atg2 wildtype condition. Analysis of segmented rim membrane features reveal surrounding and membrane-attached vesicles. The dimensions of the enlarged rims are consistent with fusion of cytosolic vesicles with the growing phagophore. High-resolution imaging in this study suggests that, apart from the initial nucleation phase, vesicle fusion can also contribute to phagophore expansion during later stages of autophagosome biogenesis.</p>","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038910","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
Chronic stress disrupts the network among stress granules, processing bodies and motor proteins. 慢性应激破坏应激颗粒、p体和运动蛋白之间的网络。
IF 3.9 3区 生物学
Journal of cell science Pub Date : 2026-09-15 Epub Date: 2026-10-01 DOI: 10.1242/jcs.264801
Yuichiro Adachi, Masashi Masuda, Yutaka Taketani, Paul J Anderson, Pavel V Ivanov
{"title":"Chronic stress disrupts the network among stress granules, processing bodies and motor proteins.","authors":"Yuichiro Adachi, Masashi Masuda, Yutaka Taketani, Paul J Anderson, Pavel V Ivanov","doi":"10.1242/jcs.264801","DOIUrl":"10.1242/jcs.264801","url":null,"abstract":"<p><p>Stress granules (SGs) are dynamic RNA condensates that assemble rapidly in response to cellular stress following translational arrest, thereby promoting adaptation and influencing disease pathogenesis. Although SG assembly and disassembly during acute stress have been extensively characterized, their regulation under chronic stress remains poorly understood. We have previously shown that chronic stress preconditioning suppresses the earliest stages of SG assembly through translation-dependent mechanisms. Whether chronic stress also impaired subsequent SG maturation remained unknown. Here, we demonstrate that chronic stress limits SG maturation by disrupting the MYH9-dependent interaction network centered on the core SG nucleator G3BP1. Loss of this interaction reduces SG size and impairs docking between SGs and processing bodies (PBs), thereby restricting the maturation of nascent SGs. In parallel, chronic stress decreases expression of the SG nucleator UBAP2L, an essential regulator of SG-PB docking, further exacerbating these defects. Together, our findings identify chronic stress as a regulator of the MYH9-G3BP1-UBAP2L axis and reveal that chronic stress inhibits SG maturation through translation-independent mechanisms.</p>","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148793578","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
Increased tissue tension caused by depletion of CLDN3 in the non-neural ectoderm causes neural tube defects in chick embryos. 非神经外胚层CLDN3缺失导致组织张力增加,导致鸡胚神经管缺陷。
IF 3.9 3区 生物学
Journal of cell science Pub Date : 2026-09-15 Epub Date: 2026-09-25 DOI: 10.1242/jcs.264758
Elizabeth-Ann Legere, Marie Dumont, Jordan A Dias, Yojiro Yamanaka, Gabriel L Galea, Aimee K Ryan
{"title":"Increased tissue tension caused by depletion of CLDN3 in the non-neural ectoderm causes neural tube defects in chick embryos.","authors":"Elizabeth-Ann Legere, Marie Dumont, Jordan A Dias, Yojiro Yamanaka, Gabriel L Galea, Aimee K Ryan","doi":"10.1242/jcs.264758","DOIUrl":"10.1242/jcs.264758","url":null,"abstract":"<p><p>Neural tube morphogenesis provides a dynamic setting in which to study epithelial cell behaviours. Here, we examined CLDN3-dependent biomechanical properties of the non-neural ectoderm during neural tube closure in chick embryos. Previous analyses of static images of chick embryos suggested that spinal neural tube closure occurs through multiple contact points or 'buttoning'. Using live imaging and transverse cuts through the neural folds we confirmed the multiple simultaneous 'buttoning' contacts along the anterior-posterior axis and showed that spinal neural fold fusion is not the result of progressive 'zippering' cell behaviours as is required in cranial and posterior neuropore regions. CLDN3 depletion decreased the rate of neural fold closure between points of contact and increased phosphorylated myosin light chain (pMLC) within the apical domain of non-neural ectoderm cells, suggesting increased actomyosin contraction. Laser ablation studies revealed that CLDN3-depleted embryos exhibited higher tension across the non-neural ectoderm during neural fold fusion. Decreasing tension with blebbistatin rescued the neural fold fusion defects in CLDN3-depleted embryos. Our data support the importance of CLDN3 to regulate tissue tension through effects on cytoskeletal dynamics in the non-neural ectoderm during neural fold fusion.</p>","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13680966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148761626","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
Reconstitution of lamin assembly on nuclear pore complex-containing membranes. 核孔复合物膜上层蛋白组装的重构。
IF 3.9 3区 生物学
Journal of cell science Pub Date : 2026-09-15 Epub Date: 2026-09-24 DOI: 10.1242/jcs.265192
Ross T A Pedersen, Yinyin Zhuang, Andres V Reyes, Shou-Ling Xu, Xiaoyu Shi, Yixian Zheng
{"title":"Reconstitution of lamin assembly on nuclear pore complex-containing membranes.","authors":"Ross T A Pedersen, Yinyin Zhuang, Andres V Reyes, Shou-Ling Xu, Xiaoyu Shi, Yixian Zheng","doi":"10.1242/jcs.265192","DOIUrl":"10.1242/jcs.265192","url":null,"abstract":"<p><p>Intermediate filaments called lamins line the metazoan nuclear envelope and organize the nucleus and genome. Unlike actin and microtubules, purified intermediate filament proteins assemble into non-physiological structures, making it difficult to connect lamin functions to their assembly and regulation. To overcome this challenge and shed light on physiological lamin assembly mechanisms, we conducted biochemical studies of lamin-B3 endogenously present in Xenopus laevis egg extract, which recapitulates physiological context. When we mimicked nucleoplasm conditions that would support assembly of lamin filaments in intact cells, lamin-B3 assembled into higher-order structures resembling filamentous meshworks without accompanying nuclear assembly. This ectopic lamin assembly occurs on nuclear pore complex-containing membranes, but does not apparently recruit known nuclear lamina components, demonstrating that a lamin assembly process is partially separable from the rest of the nuclear lamina and nucleus. This assembly assay in the physiological context of cellular components opens the door to further dissecting nuclear lamina function in nuclear organization.</p>","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758642","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
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