Pub Date : 2025-02-04DOI: 10.1016/j.devcel.2025.01.010
Jinqiu Li, Yitian Zhou, Ting Shu, Wenqi Lei, Qihao Tang, Yang Yang, Jin Zhang, Wenhui Chen, Bin Zhou, Qinghua Hu, Yanjiang Xing, Jing Wang, Chen Wang
Pulmonary vascular remodeling (PVR), encompassing microvascular loss and muscularization, contributes to multiple respiratory diseases. c-Kit+ cells exhibit differentiation potential into both endothelial cells (ECs) and smooth muscle cells. The potential role of lung c-Kit+ cell differentiation in PVR, however, remains unclear. Lung c-Kit+ cells increase in pulmonary hypertension patients and in the SU5416/hypoxia (SuHx)-induced PVR mouse model. Employing genetic lineage tracing and single-cell RNA sequencing (scRNA-seq), we elucidate that lung-resident c-Kit+ cells display an aerocyte and venular endothelial differentiation in the SuHx model. Ablation of tissue-resident c-Kit+ cells exacerbates PVR. We identify an Nr2f2-expressing c-Kit+ cell subgroup, which exhibitsvenous EC differentiation and increases during PVR. Notably, the elevation of Nr2f2 in c-Kit+ cells via AAV enhances differentiation and mitigates PVR. These findings underscore the protective role of lung tissue-resident c-Kit+ cells in PVR, achieved by differentiating into mature ECs. Targeting NR2F2 expression in c-Kit+ cells emerges as a promising strategy for reversing PVR.
{"title":"Differentiation of lung tissue-resident c-Kit+ cells into microvascular endothelial cells alleviates pulmonary vascular remodeling","authors":"Jinqiu Li, Yitian Zhou, Ting Shu, Wenqi Lei, Qihao Tang, Yang Yang, Jin Zhang, Wenhui Chen, Bin Zhou, Qinghua Hu, Yanjiang Xing, Jing Wang, Chen Wang","doi":"10.1016/j.devcel.2025.01.010","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.01.010","url":null,"abstract":"Pulmonary vascular remodeling (PVR), encompassing microvascular loss and muscularization, contributes to multiple respiratory diseases. c-Kit<sup>+</sup> cells exhibit differentiation potential into both endothelial cells (ECs) and smooth muscle cells. The potential role of lung c-Kit<sup>+</sup> cell differentiation in PVR, however, remains unclear. Lung c-Kit<sup>+</sup> cells increase in pulmonary hypertension patients and in the SU5416/hypoxia (SuHx)-induced PVR mouse model. Employing genetic lineage tracing and single-cell RNA sequencing (scRNA-seq), we elucidate that lung-resident c-Kit<sup>+</sup> cells display an aerocyte and venular endothelial differentiation in the SuHx model. Ablation of tissue-resident c-Kit<sup>+</sup> cells exacerbates PVR. We identify an <em>Nr2f2</em>-expressing c-Kit<sup>+</sup> cell subgroup, which exhibitsvenous EC differentiation and increases during PVR. Notably, the elevation of Nr2f2 in c-Kit<sup>+</sup> cells via AAV enhances differentiation and mitigates PVR. These findings underscore the protective role of lung tissue-resident c-Kit<sup>+</sup> cells in PVR, achieved by differentiating into mature ECs. Targeting NR2F2 expression in c-Kit<sup>+</sup> cells emerges as a promising strategy for reversing PVR.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"61 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143083538","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}
Pub Date : 2025-02-03DOI: 10.1016/j.devcel.2024.12.040
Anson Ming Yan Lee, Anne Schreiber
Despite limited translational capacity, senescent cells trigger inflammation by upregulating the translation and secretion of proinflammatory factors. In this issue of Developmental Cell, Kim et al. identify that altered autophagy and SFPQ-dependent EIF4H splicing during senescence redirects translation to promote inflammation, informing therapeutic strategies for cancer and other age-related diseases.
{"title":"Autophagy-dependent changes in alternative splicing bias translation toward inflammation in senescent cells","authors":"Anson Ming Yan Lee, Anne Schreiber","doi":"10.1016/j.devcel.2024.12.040","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.12.040","url":null,"abstract":"Despite limited translational capacity, senescent cells trigger inflammation by upregulating the translation and secretion of proinflammatory factors. In this issue of <em>Developmental Cell</em>, Kim et al. identify that altered autophagy and SFPQ-dependent <em>EIF4H</em> splicing during senescence redirects translation to promote inflammation, informing therapeutic strategies for cancer and other age-related diseases.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"22 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143077204","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}
Pub Date : 2025-02-03DOI: 10.1016/j.devcel.2025.01.013
Songyun Wang, Ding Xue
Most eukaryotes inherit only maternal mitochondria. The reasons for paternal mitochondrial elimination and the impacts of persistent paternal mitochondria on animals remain elusive. We show that undegraded paternal mitochondria in autophagy-deficient C. elegans embryos are gradually excluded from germ blastomeres through asymmetric partitioning during cell divisions. The embryonic cortical flow drives anterior-directed movements of paternal mitochondria and contributes to their asymmetric apportioning between two daughter blastomeres. By contrast, autophagosome-enclosed paternal mitochondria cluster around and segregate with centrosomes during mitosis and are rapidly degraded through lysosomes concentrated near centrosomes. Failure to exclude persistent paternal mitochondria from the germ blastomere at first cleavage causes their enrichment in the descendant endomesodermal (EMS) blastomere, leading to elevated reactive oxygen species levels, elongated EMS lineage durations, and increased embryonic lethality, which antioxidant treatments can suppress. Thus, regulated paternal mitochondrial distribution away from germ blastomeres is a fail-safe mechanism, protecting embryo development and maternal mitochondrial inheritance.
{"title":"Asymmetric partitioning of persistent paternal mitochondria during cell divisions safeguards embryo development and mitochondrial inheritance","authors":"Songyun Wang, Ding Xue","doi":"10.1016/j.devcel.2025.01.013","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.01.013","url":null,"abstract":"Most eukaryotes inherit only maternal mitochondria. The reasons for paternal mitochondrial elimination and the impacts of persistent paternal mitochondria on animals remain elusive. We show that undegraded paternal mitochondria in autophagy-deficient <em>C. elegans</em> embryos are gradually excluded from germ blastomeres through asymmetric partitioning during cell divisions. The embryonic cortical flow drives anterior-directed movements of paternal mitochondria and contributes to their asymmetric apportioning between two daughter blastomeres. By contrast, autophagosome-enclosed paternal mitochondria cluster around and segregate with centrosomes during mitosis and are rapidly degraded through lysosomes concentrated near centrosomes. Failure to exclude persistent paternal mitochondria from the germ blastomere at first cleavage causes their enrichment in the descendant endomesodermal (EMS) blastomere, leading to elevated reactive oxygen species levels, elongated EMS lineage durations, and increased embryonic lethality, which antioxidant treatments can suppress. Thus, regulated paternal mitochondrial distribution away from germ blastomeres is a fail-safe mechanism, protecting embryo development and maternal mitochondrial inheritance.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"28 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143077202","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}
Pub Date : 2025-02-03DOI: 10.1016/j.devcel.2025.01.003
Ece Tavukcuoglu, Gunes Esendagli
In this issue of Developmental Cell, Tang et al. identify CD74high neutrophils as a subpopulation promoted by IL-8 in the tumor microenvironment of non-small lung cancer (NSCLC). These CD74high neutrophils support anti-tumor T cell responses and enhance the efficacy of anti-PD-1 immunotherapy and targeted therapy in NSCLC.
{"title":"IL-8 contributes to functional diversity of tumor-infiltrating neutrophils: A new target for cancer immunotherapy","authors":"Ece Tavukcuoglu, Gunes Esendagli","doi":"10.1016/j.devcel.2025.01.003","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.01.003","url":null,"abstract":"In this issue of <em>Developmental Cell</em>, Tang et al. identify CD74<sup>high</sup> neutrophils as a subpopulation promoted by IL-8 in the tumor microenvironment of non-small lung cancer (NSCLC). These CD74<sup>high</sup> neutrophils support anti-tumor T cell responses and enhance the efficacy of anti-PD-1 immunotherapy and targeted therapy in NSCLC.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"35 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143077205","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}
TMC1, a unique causative gene associated with deafness, exhibits variants with autosomal dominant and recessive inheritance patterns. TMC1 codes for the transmembrane channel-like protein 1 (TMC1), a key component of the mechano-electrical transduction (MET) machinery for hearing. However, the molecular mechanism of Ca2+ regulation in MET remains unclear. Calcium and integrin-binding protein 2 (CIB2), another MET component associated with deafness, can bind with Ca2+. Our study shows that TMC1-CIB2 complex undergoes a Ca2+-induced conformational change. We identified a vertebrate-specific binding site on TMC1 that interacts with apo CIB2, linked with hearing loss. Using an ex vivo mouse organotypic cochlea model, we demonstrated that disruption of the calcium-binding site of CIB2 perturbs the MET channel conductivity. After systematically analyzing the hearing loss variants, we observed dominant mutations of TMC1 cluster around the putative ion pore or at the binding interfaces with CIB2. These findings elucidate the molecular mechanisms underlying TMC1-linked hearing loss.
{"title":"Mechano-electrical transduction components TMC1-CIB2 undergo a Ca2+-induced conformational change linked to hearing loss","authors":"Shaoxuan Wu, Lin Lin, Qiaoyu Hu, Xuebo Yao, Hongyang Wang, Shuang Liu, Qingling Liu, Yuehui Xi, Yuzhe Lin, Jianqiao Gong, Ruixing Hu, Wei Zhan, Yi Luo, Guang He, Zhijun Liu, Wei Xiong, Qiuju Wang, Zhigang Xu, Fang Bai, Qing Lu","doi":"10.1016/j.devcel.2025.01.004","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.01.004","url":null,"abstract":"<em>TMC1</em>, a unique causative gene associated with deafness, exhibits variants with autosomal dominant and recessive inheritance patterns. <em>TMC1</em> codes for the transmembrane channel-like protein 1 (TMC1), a key component of the mechano-electrical transduction (MET) machinery for hearing. However, the molecular mechanism of Ca<sup>2+</sup> regulation in MET remains unclear. Calcium and integrin-binding protein 2 (CIB2), another MET component associated with deafness, can bind with Ca<sup>2+</sup>. Our study shows that TMC1-CIB2 complex undergoes a Ca<sup>2+</sup>-induced conformational change. We identified a vertebrate-specific binding site on TMC1 that interacts with <em>apo</em> CIB2, linked with hearing loss. Using an <em>ex vivo</em> mouse organotypic cochlea model, we demonstrated that disruption of the calcium-binding site of CIB2 perturbs the MET channel conductivity. After systematically analyzing the hearing loss variants, we observed dominant mutations of TMC1 cluster around the putative ion pore or at the binding interfaces with CIB2. These findings elucidate the molecular mechanisms underlying <em>TMC1</em>-linked hearing loss.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"40 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143056429","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}
Pub Date : 2025-01-24DOI: 10.1016/j.devcel.2025.01.001
Jerry J. Fan, Anders W. Erickson, Julia Carrillo-Garcia, Xin Wang, Patryk Skowron, Xian Wang, Xin Chen, Guanqiao Shan, Wenkun Dou, Shahrzad Bahrampour, Yi Xiong, Weifan Dong, Namal Abeysundara, Michelle A. Francisco, Ronwell J. Pusong, Wei Wang, Miranda Li, Elliot Ying, Raúl A. Suárez, Hamza Farooq, Xi Huang
Distinguishing tumor maintenance genes from initiation, progression, and passenger genes is critical for developing effective therapies. We employed a functional genomic approach using the Lazy Piggy transposon to identify tumor maintenance genes in vivo and applied this to sonic hedgehog (SHH) medulloblastoma (MB). Combining Lazy Piggy screening in mice and transcriptomic profiling of human MB, we identified the voltage-gated potassium channel KCNB2 as a candidate maintenance driver. KCNB2 governs cell volume of MB-propagating cells (MPCs), with KCNB2 depletion causing osmotic swelling, decreased plasma membrane tension, and elevated endocytic internalization of epidermal growth factor receptor (EGFR), thereby mitigating proliferation of MPCs to ultimately impair MB growth. KCNB2 is largely dispensable for mouse development and KCNB2 knockout synergizes with anti-SHH therapy in treating MB. These results demonstrate the utility of the Lazy Piggy functional genomic approach in identifying cancer maintenance drivers and elucidate a mechanism by which potassium homeostasis integrates biomechanical and biochemical signaling to promote MB aggression.
{"title":"A forward genetic screen identifies potassium channel essentiality in SHH medulloblastoma maintenance","authors":"Jerry J. Fan, Anders W. Erickson, Julia Carrillo-Garcia, Xin Wang, Patryk Skowron, Xian Wang, Xin Chen, Guanqiao Shan, Wenkun Dou, Shahrzad Bahrampour, Yi Xiong, Weifan Dong, Namal Abeysundara, Michelle A. Francisco, Ronwell J. Pusong, Wei Wang, Miranda Li, Elliot Ying, Raúl A. Suárez, Hamza Farooq, Xi Huang","doi":"10.1016/j.devcel.2025.01.001","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.01.001","url":null,"abstract":"Distinguishing tumor maintenance genes from initiation, progression, and passenger genes is critical for developing effective therapies. We employed a functional genomic approach using the Lazy Piggy transposon to identify tumor maintenance genes <em>in vivo</em> and applied this to sonic hedgehog (SHH) medulloblastoma (MB). Combining Lazy Piggy screening in mice and transcriptomic profiling of human MB, we identified the voltage-gated potassium channel <em>KCNB2</em> as a candidate maintenance driver. KCNB2 governs cell volume of MB-propagating cells (MPCs), with KCNB2 depletion causing osmotic swelling, decreased plasma membrane tension, and elevated endocytic internalization of epidermal growth factor receptor (EGFR), thereby mitigating proliferation of MPCs to ultimately impair MB growth. KCNB2 is largely dispensable for mouse development and KCNB2 knockout synergizes with anti-SHH therapy in treating MB. These results demonstrate the utility of the Lazy Piggy functional genomic approach in identifying cancer maintenance drivers and elucidate a mechanism by which potassium homeostasis integrates biomechanical and biochemical signaling to promote MB aggression.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"52 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143026719","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}
Pub Date : 2025-01-24DOI: 10.1016/j.devcel.2025.01.002
Filip Vasilev, Aleksandar I. Mihajlović, Gaudeline Rémillard-Labrosse, Greg FitzHarris
Apoptosis is a key feature of preimplantation development, but whether it occurs in a cell-autonomous or coordinated manner was unknown. Here, we report that plasma membrane abscission, the final step of cell division, is profoundly delayed in early mouse embryos such that a cytokinetic bridge is maintained for the vast majority of the following interphase. Early embryos thus consist of many pairs of sister cells connected by stable cytokinetic bridges that allow them to share diffusible molecules. We show that apoptotic regulators are shared through cytokinetic bridges and that these bridges ensure that if one cell enters apoptosis, its sister cell does as well. Long-lived cytokinetic bridges are thus a previously unappreciated form of cell-cell communication within the mouse embryo that coordinate the clearance of pairs of cells with similar developmental histories.
{"title":"Long-lived cytokinetic bridges coordinate sister-cell elimination in mouse embryos","authors":"Filip Vasilev, Aleksandar I. Mihajlović, Gaudeline Rémillard-Labrosse, Greg FitzHarris","doi":"10.1016/j.devcel.2025.01.002","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.01.002","url":null,"abstract":"Apoptosis is a key feature of preimplantation development, but whether it occurs in a cell-autonomous or coordinated manner was unknown. Here, we report that plasma membrane abscission, the final step of cell division, is profoundly delayed in early mouse embryos such that a cytokinetic bridge is maintained for the vast majority of the following interphase. Early embryos thus consist of many pairs of sister cells connected by stable cytokinetic bridges that allow them to share diffusible molecules. We show that apoptotic regulators are shared through cytokinetic bridges and that these bridges ensure that if one cell enters apoptosis, its sister cell does as well. Long-lived cytokinetic bridges are thus a previously unappreciated form of cell-cell communication within the mouse embryo that coordinate the clearance of pairs of cells with similar developmental histories.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"2 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143026716","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}
Pub Date : 2025-01-21DOI: 10.1016/j.devcel.2025.01.006
Biruk A. Feyissa, Elsa M. de Becker, Coralie E. Salesse-Smith, Mengjun Shu, Jin Zhang, Timothy B. Yates, Meng Xie, Kuntal De, Dhananjay Gotarkar, Margot S.S. Chen, Sara S. Jawdy, Dana L. Carper, Kerrie Barry, Jeremy Schmutz, David J. Weston, Paul E. Abraham, Chung-Jui Tsai, Jennifer L. Morrell-Falvey, Gail Taylor, Jin-Gui Chen, Wellington Muchero
(Developmental Cell 60, 1–12.e1–e7; March 10, 2025)
(发育细胞60,1-12.e1-e7；2025年3月10日)
{"title":"An orphan gene BOOSTER enhances photosynthetic efficiency and plant productivity","authors":"Biruk A. Feyissa, Elsa M. de Becker, Coralie E. Salesse-Smith, Mengjun Shu, Jin Zhang, Timothy B. Yates, Meng Xie, Kuntal De, Dhananjay Gotarkar, Margot S.S. Chen, Sara S. Jawdy, Dana L. Carper, Kerrie Barry, Jeremy Schmutz, David J. Weston, Paul E. Abraham, Chung-Jui Tsai, Jennifer L. Morrell-Falvey, Gail Taylor, Jin-Gui Chen, Wellington Muchero","doi":"10.1016/j.devcel.2025.01.006","DOIUrl":"https://doi.org/10.1016/j.devcel.2025.01.006","url":null,"abstract":"(Developmental Cell <em>60</em>, 1–12.e1–e7; March 10, 2025)","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"28 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142990652","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}
Pub Date : 2025-01-20DOI: 10.1016/j.devcel.2024.12.018
Frederick J.H. Whiting, Trevor A. Graham
Genetic mutations cause colorectal cancer (CRC) initiation, but their contribution to metastasis and therapy resistance is less clear. In a recent issue of Nature, Moorman et al.1 use single-cell transcriptome sequencing to map the changes in cancer cell state (cell phenotypes) that occur through CRC progression.
{"title":"Plasticity in metastatic colorectal cancer","authors":"Frederick J.H. Whiting, Trevor A. Graham","doi":"10.1016/j.devcel.2024.12.018","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.12.018","url":null,"abstract":"Genetic mutations cause colorectal cancer (CRC) initiation, but their contribution to metastasis and therapy resistance is less clear. In a recent issue of <em>Nature</em>, Moorman et al.<span><span><sup>1</sup></span></span> use single-cell transcriptome sequencing to map the changes in cancer cell state (cell phenotypes) that occur through CRC progression.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"122 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142990086","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}
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