Journal of cell science最新文献

SAXO proteins mediate tubulin turnover in axonemal microtubules of Chlamydomonas. SAXO蛋白介导衣藻轴突微管中的微管蛋白转换。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-10-15 Epub Date: 2025-06-26 DOI: 10.1242/jcs.264074

Yongli Zhang, Xuecheng Li, Zhengmao Wang, Junmin Pan

{"title":"SAXO proteins mediate tubulin turnover in axonemal microtubules of Chlamydomonas.","authors":"Yongli Zhang, Xuecheng Li, Zhengmao Wang, Junmin Pan","doi":"10.1242/jcs.264074","DOIUrl":"10.1242/jcs.264074","url":null,"abstract":"Cilia and eukaryotic flagella are microtubule-based organelles that are crucial for cell motility and signaling. SAXO proteins (denoted for 'stabilizers of axonemal microtubules') are found exclusively in flagellated or ciliated organisms, but their physiological functions remain unclear. We investigated four SAXO proteins (SAXO1-SAXO4) in Chlamydomonas reinhardtii, identified via bioinformatics. All localize to cilia but differ in axonemal binding and spatial distribution. Single SAXO knockouts had no effect, whereas double mutants (saxo1/2, saxo1/3 and saxo2/3) showed shorter cilia. This phenotype intensified in the saxo1/2/3 triple mutant but not further in the quadruple mutant. Ciliary beating remained normal in saxo1/2/3 mutants, even under mechanical stress, indicating that SAXO1-SAXO3 are not essential for ciliary rigidity. Biochemical and proteomic analyses revealed no significant changes in the ciliary proteome or in tubulin acetylation, tyrosination and glutamylation within cilia. However, dikaryon assays with labeled tubulin showed that there was increased axonemal tubulin turnover in saxo1/2/3 mutant. Our findings underscore a crucial role of SAXO proteins in stabilizing axonemal microtubules by reducing tubulin turnover, thereby regulating ciliary length and assembly, and provide new insights into their function in cilia.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150414","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

Phosphorylation-induced SUMOylation promotes Ulk4 condensation at the ciliary tip to transduce Hedgehog signal. 磷酸化诱导的SUMOylation促进Ulk4在纤毛尖端的缩聚，从而转导Hedgehog信号。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-10-15 Epub Date: 2025-05-19 DOI: 10.1242/jcs.263695

Mengmeng Zhou, Yuhong Han, Jin Jiang

{"title":"Phosphorylation-induced SUMOylation promotes Ulk4 condensation at the ciliary tip to transduce Hedgehog signal.","authors":"Mengmeng Zhou, Yuhong Han, Jin Jiang","doi":"10.1242/jcs.263695","DOIUrl":"10.1242/jcs.263695","url":null,"abstract":"Hedgehog (Hh) signaling controls embryonic development and adult tissue homeostasis through the Gli family of transcription factors. In vertebrates, Hh signal transduction depends on the primary cilium, where Gli proteins are thought to be activated at the ciliary tip, but the underlying mechanism has remained poorly understood. Here, we provide evidence that two Unc-51-like kinase (Ulk) family members, Stk36 and Ulk4, regulate Gli2 ciliary tip localization and activation through phosphorylation and SUMOylation-mediated condensation in response to the Hh family protein Shh. We find that Stk36-mediated phosphorylation of Ulk4 promotes its SUMOylation in response to Shh, and the subsequent interaction between SUMO and a SUMO-interacting-motif (SIM) in the C-terminal region of Ulk4 drives Ulk4 self-assembly to form biomolecular condensates that also recruit Stk36 and Gli2. SUMOylation or SIM-deficient Ulk4 failed to accumulate at ciliary tip to activate Gli2 whereas phospho-mimetic mutation of Ulk4 sufficed to drive Ulk4, Stk36 and Gli2 condensation at ciliary tip, leading to constitutive Shh pathway activation in a manner dependent on Ulk4 SUMOylation. Taken together, our results suggest that phosphorylation-dependent SUMOylation of Ulk4 promotes kinase-substrate condensation at ciliary tip to transduce the Hh signal.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12148026/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764075","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

Skeletal ciliopathy variants of the dynein-2 DYNC2LI1 subunit impair osteogenic differentiation of mesenchymal stem cells. 骨骼肌纤毛病动力蛋白-2 DYNC2LI1亚基变异损害间充质干细胞的成骨分化。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-10-15 Epub Date: 2025-06-20 DOI: 10.1242/jcs.263737

Yamato Ishida, Haruka Hoshi, Kenichi Kawano, Hye-Won Shin, Yohei Katoh, Kazuhisa Nakayama

{"title":"Skeletal ciliopathy variants of the dynein-2 DYNC2LI1 subunit impair osteogenic differentiation of mesenchymal stem cells.","authors":"Yamato Ishida, Haruka Hoshi, Kenichi Kawano, Hye-Won Shin, Yohei Katoh, Kazuhisa Nakayama","doi":"10.1242/jcs.263737","DOIUrl":"10.1242/jcs.263737","url":null,"abstract":"Skeletal ciliopathies result from defects in primary cilia, which are crucial for embryonic development because they transduce extracellular signals, including Hedgehog. Selective transport of ciliary proteins is mediated by the intraflagellar transport (IFT) machinery, containing the IFT-A and IFT-B complexes and the kinesin-2 and dynein-2 motors. Biallelic loss-of-function variants in genes encoding dynein-2-specific subunits, including DYNC2LI1, cause skeletal ciliopathies. As mesenchymal stem cells (MSCs) differentiate into osteoblasts, we investigated the effects of pathogenic variants of DYNC2LI1 on osteogenic differentiation of the MSC-like line C3H10T1/2. Dync2li1-knockout cells expressing disease-causing DYNC2LI1 variants demonstrated defects in the retrograde ciliary protein trafficking, including Hedgehog pathway GPCRs, Smoothened and GPR161. Furthermore, Dync2li1-knockout cells expressing the pathogenic variants demonstrated impaired Hedgehog signaling, in particular, a reduced ratio of the GLI3 repressor form to total GLI3, resulting in impaired osteogenic differentiation of MSCs. By contrast, osteogenic differentiation via BMP signaling was derepressed in Dync2li1-knockout cells. This suggests that skeletal ciliopathies caused by DYNC2LI1 variants could be attributable in part to impaired osteogenic differentiation due to defects in Hedgehog signaling, resulting from defects in retrograde ciliary protein trafficking.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110669","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

β-Arrestin mediates the export of ciliary GPR161 but not Smoothened together with the BBSome and intraflagellar transport machinery. β- arrest介导睫状GPR161的输出，但不与BBSome和IFT机制一起平滑。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-10-15 Epub Date: 2025-06-20 DOI: 10.1242/jcs.263793

Taiju Fujii, Norihito Murai, Shinya Aso, Hiroyuki Takatsu, Hye-Won Shin, Yohei Katoh, Kazuhisa Nakayama

{"title":"β-Arrestin mediates the export of ciliary GPR161 but not Smoothened together with the BBSome and intraflagellar transport machinery.","authors":"Taiju Fujii, Norihito Murai, Shinya Aso, Hiroyuki Takatsu, Hye-Won Shin, Yohei Katoh, Kazuhisa Nakayama","doi":"10.1242/jcs.263793","DOIUrl":"10.1242/jcs.263793","url":null,"abstract":"Specific G-protein-coupled receptors (GPCRs) exist on the ciliary membrane. Hedgehog signaling activation triggers the import of Smoothened into and export of GPR161 from cilia. The BBSome, which comprises eight Bardet-Biedl syndrome (BBS) proteins, mediates GPCR export, together with the intraflagellar transport (IFT) machinery, containing the IFT-A and IFT-B complexes. The absence of any BBSome subunit or IFT27 (also known as BBS19) (an IFT-B subunit) impairs ciliary GPCR export, including that of GPR161. Plasma membrane GPCRs undergo phosphorylation by GPCR kinases (GRKs) and subsequent binding of β-arrestins [β-arrestin1 (ARRB1) and β-arrestin2 (ARRB2)], which is crucial for clathrin-mediated endocytosis. We here confirmed that GPR161 and β-arrestin are accumulated within cilia in the absence of IFT27 or the BBSome, and that ARRB1 and ARRB2 double-knockout impairs GPR161 export. Notably, we found that activation-mimetic β-arrestin mutants can interact with both the BBSome and ciliary GPCRs, and cause constitutive export of GPR161. Moreover, we demonstrated that GRK2 plays a crucial role in GPR161 export. We here propose that phosphorylated GPR161 recruits β-arrestins, converting them into their activated conformation. Activated β-arrestins then interact with the BBSome, which connects them to the IFT machinery to facilitate GPR161 export.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093707","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

Primary cilia shape postnatal astrocyte development through Sonic Hedgehog signaling. 初级纤毛通过Sonic Hedgehog信号影响出生后星形胶质细胞的发育。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-10-15 Epub Date: 2025-05-19 DOI: 10.1242/jcs.263965

Rachel Bear, Steven A Sloan, Tamara Caspary

{"title":"Primary cilia shape postnatal astrocyte development through Sonic Hedgehog signaling.","authors":"Rachel Bear, Steven A Sloan, Tamara Caspary","doi":"10.1242/jcs.263965","DOIUrl":"10.1242/jcs.263965","url":null,"abstract":"Primary cilia function as specialized signaling centers that regulate many cellular processes including neuron and glia development. Astrocytes possess cilia, but the function of cilia in astrocyte development remains largely unexplored. Crucially, dysfunction of either astrocytes or cilia contributes to the molecular changes observed in neurodevelopmental disorders. Here, we show that a subpopulation of developing astrocytes in the prefrontal cortex are ciliated. This population corresponds to proliferating astrocytes and largely expresses the ciliary protein ARL13B. Genetic ablation of astrocyte cilia in vivo at two distinct stages of astrocyte development results in changes to Sonic Hedgehog (Shh) transcriptional targets. We show that Shh activity is decreased in immature and mature astrocytes upon loss of cilia. Furthermore, loss of cilia in immature astrocytes results in decreased astrocyte proliferation and loss of cilia in mature astrocytes causes enlarged astrocyte morphology. Together, these results indicate that astrocytes require cilia for Shh signaling throughout development and uncover functions for astrocyte cilia in regulating astrocyte proliferation and maturation. This expands our fundamental knowledge of astrocyte development and cilia function to advance our understanding of neurodevelopmental disorders.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12148023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663530","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

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 : 2025-06-27 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":"https://doi.org/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 (Hef1, NEDD9) as a central regulator of integrin-dependent migration in primary T cells. We found CasL is specifically needed for efficient migration on ICAM-1, but not VCAM-1 coated surfaces. While WT T cells migrating on ICAM-1 form an actin-rich cell front and move smoothly, T cells lacking CasL instead form 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 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":"2025-06-27","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

14-3-3ɛ 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 : 2025-06-27 DOI: 10.1242/jcs.263808

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

{"title":"14-3-3ɛ 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":"https://doi.org/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 14-3-3ɛ regulates centrosome duplication, we altered two conserved acidic residues in the 14-3-3ɛ 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, while cells expressing the E134A mutant showed the presence of supernumerary centrosomes. We demonstrate that 14-3-3ɛ 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 14-3-3ɛ inhibits the activity of Plk1 and Separase, 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 disrupting complex formation between 14-3-3ɛ 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":"2025-06-27","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

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 : 2025-06-25 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":"https://doi.org/10.1242/jcs.263897","url":null,"abstract":"A/B toxins are a diverse family of protein toxins that enter host cells via endocytosis and induce cell death. In yeast, the A/B 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 to 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 may survey endolysosomal compartments for toxin. This work underpins the importance of Ktd1 in defence against the A/B 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":"2025-06-25","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

Inhibition of Hedgehog signaling does not mitigate polycystic kidney disease severity in a Pkd1 mutant mouse model. 在Pkd1突变小鼠模型中，抑制刺猬信号传导不能减轻多囊肾病的严重程度。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-06-23 DOI: 10.1242/jcs.264133

Sean Gombart, Scott Houghtaling, Tzu-Hua Ho, David R Beier

引用次数: 0

Proteasome-dependent Orc6 removal from chromatin upon S-phase entry safeguards against MCM reloading and tetraploidy. 在s期进入时，蛋白酶体依赖的Orc6从染色质上去除，防止MCM重新加载和四倍体。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2025-06-18 DOI: 10.1242/jcs.263596

Yoko Hayashi-Takanaka, Ichiro Hiratani, Tokuko Haraguchi, Yasushi Hiraoka

{"title":"Proteasome-dependent Orc6 removal from chromatin upon S-phase entry safeguards against MCM reloading and tetraploidy.","authors":"Yoko Hayashi-Takanaka, Ichiro Hiratani, Tokuko Haraguchi, Yasushi Hiraoka","doi":"10.1242/jcs.263596","DOIUrl":"https://doi.org/10.1242/jcs.263596","url":null,"abstract":"DNA replication is tightly regulated to occur only once per cell cycle, as untimely re-initiation can lead to aneuploidy, which is associated with early senescence and cancer. The pre-replication complex (comprising Orc1-6, Cdc6, Cdt1, and MCM) is essential for the initiation of DNA replication, but the dynamics and function of Orc6 during the cell cycle remain elusive. Here, we demonstrate that Orc6 associates with chromatin during G1-phase and dissociates upon S-phase entry. The dissociation of Orc6 from chromatin is dependent on proteasome activity, and inhibition of the proteasome leads to the accumulation of chromatin-bound Orc6, which promotes abnormal MCM loading after S-phase entry without undergoing mitosis in human immortalized hTERT-RPE1 cells. Following release from proteasome inhibition, cells with elevated levels of chromatin-bound Orc6 and MCM proceed to the next replication phase as tetraploid cells. Our findings suggest that the proteasome-dependent dissociation of Orc6 after DNA replication is critical for preventing inappropriate MCM reloading and tetraploid formation.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144484532","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