Journal of cell science最新文献_第2页

Cell cycle- and dose-dependent effects on mitochondrial DNA copy number variation following irradiation. 细胞周期和剂量依赖性对辐照后线粒体DNA拷贝数变异的影响。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-07-18 DOI: 10.1242/jcs.263642

Ryosuke Seino, Kai Nishikubo, Hisanori Fukunaga

引用次数: 0

Front-biased activation of Ras-Rab5-Rac1 loop coordinates collective cell migration. Ras-Rab5-Rac1环的前偏置激活协调了细胞的集体迁移。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-07-16 DOI: 10.1242/jcs.263779

Yuya Jikko, Eriko Deguchi, Kimiya Matsuda, Naoya Hino, Shinya Tsukiji, Michiyuki Matsuda, Kenta Terai

{"title":"Front-biased activation of Ras-Rab5-Rac1 loop coordinates collective cell migration.","authors":"Yuya Jikko, Eriko Deguchi, Kimiya Matsuda, Naoya Hino, Shinya Tsukiji, Michiyuki Matsuda, Kenta Terai","doi":"10.1242/jcs.263779","DOIUrl":"https://doi.org/10.1242/jcs.263779","url":null,"abstract":"Collective cell migration is coordinated by the front-to-rear intercellular propagation of EGFR-Ras-ERK pathway activation. However, the molecular mechanisms integrating front-to-rear information into this intercellular signaling cascade, particularly the determinants of cellular front-side specification, remain elusive. We visualized the activity of EGFR, Ras, Rac1, and Rab5 by using FRET biosensors and chemogenetic tools. While EGFR activation was uniformly observed within cells, Ras activation was biased to the front side within cells. The polarized Ras activation depended on Merlin and Rac1, which also showed front-biased activation. Furthermore, Rab5, a crucial regulator of cell migration, demonstrated similar front-biased activation and was found to function downstream of Ras while being necessary for Rac1 activation. Thus, the positive feedback loop consisting of Ras, Rab5, and Rac1 is activated primarily at the front of collectively migrating cells. These findings offer new spatio-temporal insight into processing front-rear information during collective cell migration.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642638","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

Killer toxin K28 resistance in yeast relies on COG complex-mediated trafficking of the defence factor Ktd1. 酵母对杀伤毒素K28的抗性依赖于COG复合物介导的防御因子Ktd1的转运。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-07-15 Epub Date: 2025-07-18 DOI: 10.1242/jcs.263897

Kamilla M E Laidlaw, Hatwan H Nadir, Amy Milburn, Martha S C Xelhuantzi, Justas Stanislovas, Alastair P Droop, Sandy MacDonald, Ilya Andreev, Andrew Leech, Daniel Ungar, Meru J Sadhu, Chris MacDonald

{"title":"Killer toxin K28 resistance in yeast relies on COG complex-mediated trafficking of the defence factor Ktd1.","authors":"Kamilla M E Laidlaw, Hatwan H Nadir, Amy Milburn, Martha S C Xelhuantzi, Justas Stanislovas, Alastair P Droop, Sandy MacDonald, Ilya Andreev, Andrew Leech, Daniel Ungar, Meru J Sadhu, Chris MacDonald","doi":"10.1242/jcs.263897","DOIUrl":"10.1242/jcs.263897","url":null,"abstract":"AB toxins are a diverse family of protein toxins that enter host cells via endocytosis and induce cell death. In yeast, the AB toxin K28 is internalised to endosomes of susceptible yeast, before following the retrograde trafficking pathway and ultimately triggering cell cycle arrest. The endolysosomal defence factor Ktd1 protects against K28, but its regulation remains unclear. We show all lobe B subunits of the conserved oligomeric Golgi (COG) tethering complex are required for K28 resistance. Our experiments suggest the hypersensitivity of cog mutants is primarily explained by defects in Ktd1 trafficking. Ktd1 mis-localisation in cog mutants is reminiscent of disruptions in Snc1, a surface cargo that recycles multiple times via the Golgi. This work suggests not only that the COG complex is responsible for the precise trafficking of Ktd1 required to mediate toxin defence, but that Ktd1 might survey endolysosomal compartments for toxin. This work underpins the importance of Ktd1 in defence against the AB toxin K28, and implies how various membrane trafficking regulators could influence toxin effects in other eukaryotic systems.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144484531","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

CLASP1 regulates DYNC1I1 for PLK1-mediated spindle organization and cytokinesis in oocyte meiosis. CLASP1在卵母细胞减数分裂中调控plk1介导的纺锤体组织和细胞分裂的动力蛋白。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-07-15 Epub Date: 2025-07-22 DOI: 10.1242/jcs.264015

Meng-Meng Shan, Ping-Shuang Lu, Yuan-Jing Zou, Kun-Huan Zhang, Jing-Cai Liu, Jia-Qian Ju, Shao-Chen Sun

{"title":"CLASP1 regulates DYNC1I1 for PLK1-mediated spindle organization and cytokinesis in oocyte meiosis.","authors":"Meng-Meng Shan, Ping-Shuang Lu, Yuan-Jing Zou, Kun-Huan Zhang, Jing-Cai Liu, Jia-Qian Ju, Shao-Chen Sun","doi":"10.1242/jcs.264015","DOIUrl":"10.1242/jcs.264015","url":null,"abstract":"Meiotic spindle organization and cytokinesis are important for mammalian oocyte maturation. CLIP-associating protein 1 (CLASP1) is a member of the microtubule plus-end-binding proteins that has been reported to regulate cytokinesis in mitosis; however, the functions of CLASP1 in meiosis are still unclear. In this study, we found that CLASP1 plays critical roles both at metaphase and telophase in mouse oocyte meiosis. Our results indicated that CLASP1 is essential for oocyte maturation. Its knockdown caused spindle organization defects and microtubule-kinetochore-attachment defects at metaphase I, which might be due to its association with polo-like kinase 1 (PLK1) and/or phosphorylated mitogen-activated protein kinases (MAPKs), specifically phosphorylated MAPK1 and MAPK3. Furthermore, the levels of deacetylases, i.e. histone deacetylase 6 (HDAC6) and/or NAD-dependent protein deacetylase sirtuin-1 (SIRT1), were found to be increased, which further affected tubulin acetylation levels and microtubule stability after CLASP1 knockdown. We also showed that CLASP1 can associate with PLK1 and/or protein regulator of cytokinesis 1 (PRC1)-based central spindle formation and cytokinesis at telophase I. Moreover, cytoplasmic dynein 1 intermediate chain 1 (DYNC1I1) was recognized to interact closely with CLASP1 and may function as a downstream motor protein involved in the orderly transport of PLK1. Taken together, we demonstrated that CLASP1 may associate with DYNC1I1 to play multiple roles in PLK1-mediated spindle organization and cytokinesis in mouse oocyte meiosis.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274964","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

ATP synthase epsilon subunit is an unconventional adaptor in clathrin-mediated endocytosis of hemoglobin in Leishmania. ATP合成酶epsilon亚基：利什曼原虫中网格蛋白介导的血红蛋白内吞作用的非常规适配器。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-07-15 Epub Date: 2025-07-24 DOI: 10.1242/jcs.263555

Anjali Kapoor, Jitender Kumar Verma, Deepali Goyal, Shruti Agarwal, Aditi Gaur, Amitabha Mukhopadhyay

{"title":"ATP synthase epsilon subunit is an unconventional adaptor in clathrin-mediated endocytosis of hemoglobin in Leishmania.","authors":"Anjali Kapoor, Jitender Kumar Verma, Deepali Goyal, Shruti Agarwal, Aditi Gaur, Amitabha Mukhopadhyay","doi":"10.1242/jcs.263555","DOIUrl":"10.1242/jcs.263555","url":null,"abstract":"In clathrin-mediated endocytosis, the cytoplasmic domain of the receptor binds to the AP2 adaptor, which recruits clathrin to mediate endocytosis. The classical AP2 adaptor in Leishmania has not yet been characterized. Here, we identified ATP synthase epsilon (LdATPSε) subunit as a novel adaptor in Leishmania using yeast two-hybrid screening. Subsequently, we cloned and expressed LdATPSε from Leishmania and showed that LdATPSε colocalizes with LdClathrin and the hemoglobin receptor in Leishmania. We found that LdATPSε directly binds to a cargo-binding motif, 'YLAP', in the cytoplasmic domain of the high-affinity hemoglobin receptor, whereas it interacts with the LdClathrin terminal domain via a clathrin-binding motif, 'LSELD'. Consequently, we showed that mutated clathrin binding box LdATPSεL133A/L136A/D137A does not bind to clathrin and fails to localize in the flagellar pocket, and its overexpression completely blocks hemoglobin internalization in Leishmania. LdATPSε-/- parasites are not viable, indicating the essential function of LdATPSε. However, hemoglobin internalization in LdATPSε+/- parasites is significantly blocked, and LdATPSε+/- parasites fail to grow in macrophages as the parasites are unable to internalize hemoglobin. Our results demonstrate that LdATPSε is a novel adaptor for clathrin in hemoglobin endocytosis in Leishmania.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144484529","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

Reinterpreting the effects of α-tubulin K40 acetylation on microtubule stability and cellular functions. 重新解释α-微管蛋白K40乙酰化对微管稳定性和细胞功能的影响。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-07-15 DOI: 10.1242/jcs.263431

Yu-Ming Lu

{"title":"Reinterpreting the effects of α-tubulin K40 acetylation on microtubule stability and cellular functions.","authors":"Yu-Ming Lu","doi":"10.1242/jcs.263431","DOIUrl":"10.1242/jcs.263431","url":null,"abstract":"Acetylation of α-tubulin at lysine 40 (K40) has been studied in many model organisms for decades, mainly by manipulating levels of deacetylase and acetyltransferase enzymes, such as the α-tubulin acetyltransferase MEC-17 (also known as ATAT1). Observations that acetylation accumulates in some long-lived microtubules and that MEC-17 is important for maintaining microtubule organization and key cellular functions have led to the prevailing view that K40 acetylation stabilizes and protects microtubules, although many questions about its precise function remain. Recent gene editing of endogenous α-tubulin and in vitro microtubule polymerization assays have indicated that K40 acetylation itself does not maintain microtubule structure as MEC-17 does, but rather negatively regulates specific aspects of microtubule dynamics (i.e. nucleation and shrinkage but not elongation) and slightly impairs neuronal extension. This Opinion article discusses multiple important studies on α-tubulin K40 acetylation that have shaped our understanding of its function since its discovery in the 1980s, with the aim of clarifying the actual role of this major tubulin post-translational modification.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":"138 14","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642639","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

The scaffold protein CasL restrains membrane blebbing and promotes T cell migration. 支架蛋白CasL抑制膜起泡，促进T细胞迁移。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-07-15 Epub Date: 2025-07-18 DOI: 10.1242/jcs.263792

Liz A Kurtz, Hope E Shearer, Rosanne Trevail, Menelaos Symeonides, Mobin Karimi, Nathan H Roy

{"title":"The scaffold protein CasL restrains membrane blebbing and promotes T cell migration.","authors":"Liz A Kurtz, Hope E Shearer, Rosanne Trevail, Menelaos Symeonides, Mobin Karimi, Nathan H Roy","doi":"10.1242/jcs.263792","DOIUrl":"10.1242/jcs.263792","url":null,"abstract":"T cell migration into inflamed tissue is a key control point in the inflammatory response and relies on integrin interactions with their endothelial ligands. Here, we identify the signaling scaffold CasL (also known as Hef1 and NEDD9) as a central regulator of integrin-dependent migration in primary T cells. We found that CasL is specifically needed for efficient migration on ICAM-1-, but not VCAM-1-coated surfaces. Although wild-type T cells migrating on ICAM-1 formed an actin-rich cell front and move smoothly, T cells lacking CasL instead formed numerous, aberrant membrane blebs. CasL was needed for the normal distribution of F-actin in the cell front and phosphorylated myosin light chain in the cell rear, suggesting that CasL regulates the cytoskeletal architecture in migrating T cells. Importantly, using an in vivo allogeneic hematopoietic transplant model, we found that CasL promotes T cell migration into inflamed peripheral tissue, but was dispensable for trafficking to secondary lymphoid organs. Together, these results indicate CasL functions to control the balance of cytoskeletal components during integrin-dependent migration and highlight the importance of integrin signaling for proper migration into inflamed tissue.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505769","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

14-3-3ε inhibits premature centriole disengagement by inhibiting the activity of Plk1 and separase. 14-3-3通过抑制Plk1和分离酶活性抑制中心粒过早脱离。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-07-15 Epub Date: 2025-07-18 DOI: 10.1242/jcs.263808

Monika A Jaiswal, Akshay Karn, Aparna Das, Anisha Kumari, Shilu Tiwari, Sorab N Dalal

{"title":"14-3-3ε inhibits premature centriole disengagement by inhibiting the activity of Plk1 and separase.","authors":"Monika A Jaiswal, Akshay Karn, Aparna Das, Anisha Kumari, Shilu Tiwari, Sorab N Dalal","doi":"10.1242/jcs.263808","DOIUrl":"10.1242/jcs.263808","url":null,"abstract":"The 14-3-3 protein family regulates several pathways in mammalian cells, including centrosome duplication. However, the precise mechanisms by which 14-3-3 paralogs regulate the centrosome cycle remain unclear. To identify the mechanisms by which 14-3-3ε regulates centrosome duplication, we altered two conserved acidic residues in the 14-3-3ε phospho-peptide-binding pocket that regulate complex formation and dissociation with the associated ligands, D127 and E134, to alanine. Altering these residues to alanine led to opposing effects on centrosome duplication; the D127A mutant inhibited centrosome duplication, whereas cells expressing the E134A mutant showed the presence of supernumerary centrosomes. We demonstrate that 14-3-3ε does not inhibit centriole duplication, as reported for 14-3-3γ, but inhibits centriole disengagement. Using a combination of pharmacological and genetic approaches, we demonstrate that 14-3-3ε inhibits the activity of Plk1 and separase [also known as separin (ESPL1)], leading to disengagement defects that ultimately lead to decreased proliferation and cell death. Our work demonstrates that different 14-3-3 paralogs regulate different steps in the centrosome cycle and that disrupting complex formation between 14-3-3ε and Plk1 or separase could be a novel therapeutic strategy in tumor cells.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505768","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

Somatic mutations in IRE1α regulate keratinocyte migration and survival by differentially activating Rho GTPases. IRE1α体细胞突变通过差异激活Rho gtpase调节角质形成细胞的迁移和存活。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-07-14 DOI: 10.1242/jcs.263790

Saie Mogre, Lily Robinson, Komal Sethia, Bipin Rimal, Jeongin Son, Christian Pacifico, Lorraine Santy, Andrew Patterson, Adam B Glick

{"title":"Somatic mutations in IRE1α regulate keratinocyte migration and survival by differentially activating Rho GTPases.","authors":"Saie Mogre, Lily Robinson, Komal Sethia, Bipin Rimal, Jeongin Son, Christian Pacifico, Lorraine Santy, Andrew Patterson, Adam B Glick","doi":"10.1242/jcs.263790","DOIUrl":"https://doi.org/10.1242/jcs.263790","url":null,"abstract":"IRE1α is an Endoplasmic Reticulum (ER) transmembrane protein with cytoplasmic kinase and endoribonuclease (RNase) domains. Under ER stress, IRE1α can splice Xbp1 mRNA enabling translation of this Unfolded Protein Response transcription factor or mediate sequence-specific degradation of mRNAs through Regulated IRE1α-Dependent Decay (RIDD). Somatic mutations in IRE1α occur in many different human cancers including non-melanoma skin cancers (NMSC). To understand their role in skin cancer pathogenesis, we generated immortalized primary mouse keratinocytes inducibly expressing multiple engineered and cancer-associated mutations, including those present in NMSC. All NMSC mutations tested were activating mutations with elevated autophosphorylation and enhanced RIDD activity relative to Xbp1 splicing. Pathway analysis of RNA-Seq data and in vitro studies showed that RNase-impaired mutations enhanced cell migration due to increased levels of active RhoA and a RIDD target, Angptl4. In contrast, activating mutations exhibited elevated Rac1 activation, enrichment of genes involved in DNA repair, increased phospho-ATR levels, and improved survival in response to UVB irradiation, a critical etiological factor for sun-exposed skin cancers. Together, these results suggest divergent roles of IRE1α mutations by mediating critical tumor-promoting events in keratinocytes.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626413","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

Syntaxin-2 balances phagocytic uptake and phagolysosomal clearance in macrophages. Syntaxin-2在巨噬细胞中平衡吞噬摄取和吞噬溶酶体清除。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-07-11 DOI: 10.1242/jcs.263855

Suman Samanta, Abhrajyoti Nandi, Rupak Datta, Subhankar Dolai

{"title":"Syntaxin-2 balances phagocytic uptake and phagolysosomal clearance in macrophages.","authors":"Suman Samanta, Abhrajyoti Nandi, Rupak Datta, Subhankar Dolai","doi":"10.1242/jcs.263855","DOIUrl":"https://doi.org/10.1242/jcs.263855","url":null,"abstract":"Phagocytosis engulfs receptor-bound particles within phagosomes that mature into acidic, hydrolase-enriched phagolysosomes for content degradation. While an essential process for host defense and homeostasis, defective or uncontrolled phagocytosis can be detrimental. We report here, syntaxin-2 (Stx2), a poorly characterized SNARE in phagocytes, define the course of macrophage phagocytosis by coordinating surface receptor density, phagosome biogenesis, and maturation. Stx2 is expressed primarily on the plasma membrane, early endosomes and phagosomes. Stx2 knockdown (Stx2-KD) increases entrapment and uptake of IgG-opsonized particles by dysregulated formation and expansion of phagocytic cups, driven by elevated IgG receptor recycling and trafficking of early endosomes and VAMP4-positive post-Golgi compartments to phagocytic cups. Interestingly, Stx2-KD decreases secretion of pro-cathepsins and increases lysosome content. However, Stx2-KD impedes phagosome maturation by preventing coalescence with late endosomes, lysosomes, and reducing phagosomal acidification. Consequently, Stx2-depleted macrophages exhibit aberrant uptake of IgG-opsonized bacteria and impaired digestion, resulting in increased intracellular accumulation of intact bacteria. Collectively, Stx2 critically balances phagocytic uptake and phagolysosomal clearance in macrophages, suggesting Stx2 could be an attractive target to modulate phagocytosis plasticity and to control aberrant phagocytosis.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608497","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