European journal of cell biology最新文献

{"title":"Call to action to properly utilize electron microscopy to measure organelles to monitor disease","authors":"Kit Neikirk ,&nbsp;Edgar-Garza Lopez ,&nbsp;Andrea G. Marshall ,&nbsp;Ahmad Alghanem ,&nbsp;Evan Krystofiak ,&nbsp;Bartosz Kula ,&nbsp;Nathan Smith ,&nbsp;Jianqiang Shao ,&nbsp;Prasanna Katti ,&nbsp;Antentor Hinton Jr.","doi":"10.1016/j.ejcb.2023.151365","DOIUrl":"10.1016/j.ejcb.2023.151365","url":null,"abstract":"<div><p>This review provides an overview of the current methods for quantifying mitochondrial ultrastructure, including cristae morphology, mitochondrial contact sites, and recycling machinery and a guide to utilizing electron microscopy to effectively measure these organelles. Quantitative analysis of mitochondrial ultrastructure is essential for understanding mitochondrial biology and developing therapeutic strategies for mitochondrial-related diseases. Techniques such as transmission electron microscopy (TEM) and serial block face-scanning electron microscopy, as well as how they can be combined with other techniques including confocal microscopy, super-resolution microscopy, and correlative light and electron microscopy are discussed. Beyond their limitations and challenges, we also offer specific magnifications that may be best suited for TEM analysis of mitochondrial, endoplasmic reticulum, and recycling machinery. Finally, perspectives on future quantification methods are offered.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151365"},"PeriodicalIF":6.6,"publicationDate":"2023-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49675868","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}

{"title":"A bacterial effector protein promotes nuclear translocation of Stat3 to induce IL-10","authors":"Laura Berneking,&nbsp;Indra Bekere,&nbsp;Sören Rob,&nbsp;Marie Schnapp,&nbsp;Jiabin Huang,&nbsp;Klaus Ruckdeschel,&nbsp;Martin Aepfelbacher","doi":"10.1016/j.ejcb.2023.151364","DOIUrl":"10.1016/j.ejcb.2023.151364","url":null,"abstract":"<div><p>The multifunctional <em>Yersinia</em> effector YopM inhibits effector triggered immunity and increases production of the anti-inflammatory cytokine Interleukin-10 (IL-10) to suppress the host immune response. Previously it was shown that YopM induces IL-10 gene expression by elevating phosphorylation of the serine-threonine kinase RSK1 in the nucleus of human macrophages. Using transcriptomics, we found that YopM strongly affects expression of genes belonging to the JAK-STAT signaling pathway. Further analysis revealed that YopM mediates nuclear translocation of the transcription factor Stat3 in <em>Y. enterocolitica</em> infected macrophages and that knockdown of Stat3 inhibited YopM-induced IL-10 gene expression. YopM-induced Stat3 translocation did not depend on autocrine IL-10, activation of RSK1 or tyrosine phosphorylation of Stat3. Thus, besides activation of RSK1, stimulation of nuclear translocation of Stat3 is another mechanism by which YopM increases IL-10 gene expression in macrophages.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151364"},"PeriodicalIF":6.6,"publicationDate":"2023-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41129413","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}

{"title":"Purification of modified mammalian actin isoforms for in vitro reconstitution assays","authors":"David J. Kast,&nbsp;Silvia Jansen","doi":"10.1016/j.ejcb.2023.151363","DOIUrl":"10.1016/j.ejcb.2023.151363","url":null,"abstract":"<div><p>In vitro reconstitution assays using purified actin have greatly improved our understanding of cytoskeletal dynamics and their regulation by actin-binding proteins. However, early purification methods consisted of harsh conditions to obtain pure actin and often did not include correct maturation and obligate modification of the isolated actin monomers. Novel insights into the folding requirements and N-terminal processing of actin as well as a better understanding of the interaction of actin with monomer sequestering proteins such as DNaseI, profilin and gelsolin, led to the development of more gentle approaches to obtain pure recombinant actin isoforms with known obligate modifications. This review summarizes the approaches that can be employed to isolate natively folded endogenous and recombinant actin from tissues and cells. We further emphasize the use and limitations of each method and describe how these methods can be implemented to study actin PTMs, disease-related actin mutations and novel actin-like proteins.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151363"},"PeriodicalIF":6.6,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41102505","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}

{"title":"Concept of lipid droplet biogenesis","authors":"R.Mankamna Kumari ,&nbsp;Amit Khatri ,&nbsp;Ritika Chaudhary,&nbsp;Vineet Choudhary","doi":"10.1016/j.ejcb.2023.151362","DOIUrl":"10.1016/j.ejcb.2023.151362","url":null,"abstract":"<div><p>Lipid droplets (LD) are functionally conserved fat storage organelles found in all cell types. LDs have a unique structure comprising of a hydrophobic core of neutral lipids (fat), triacylglycerol (TAG) and cholesterol esters (CE) surrounded by a phospholipid monolayer. LD surface is decorated by a multitude of proteins and enzymes rendering this compartment functional. Accumulating evidence suggests that LDs originate from discrete ER-subdomains, demarcated by the lipodystrophy protein seipin, however, the mechanisms of which are not well understood. LD biogenesis factors together with biophysical properties of the ER membrane orchestrate spatiotemporal regulation of LD nucleation and growth at specific ER subdomains in response to metabolic cues. Defects in LD formation manifests in several human pathologies, including obesity, lipodystrophy, ectopic fat accumulation, and insulin resistance. Here, we review recent advances in understanding the molecular events during initial stages of eukaryotic LD assembly and discuss the critical role of factors that ensure fidelity of this process.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151362"},"PeriodicalIF":6.6,"publicationDate":"2023-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41111831","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}

{"title":"Loss of mfsd8 alters the secretome during Dictyostelium aggregation","authors":"Robert J. Huber ,&nbsp;Joshua Gray ,&nbsp;William D. Kim","doi":"10.1016/j.ejcb.2023.151361","DOIUrl":"10.1016/j.ejcb.2023.151361","url":null,"abstract":"<div><p>Major facilitator superfamily domain-containing protein 8 (MFSD8) is a transmembrane protein that has been reported to function as a lysosomal chloride channel. In humans, homozygous mutations in <em>MFSD8</em> cause a late-infantile form of neuronal ceroid lipofuscinosis (NCL) called CLN7 disease. In the social amoeba <em>Dictyostelium discoideum</em>, Mfsd8 localizes to cytoplasmic puncta and vesicles, and regulates conserved processes during the organism’s life cycle. Here, we used <em>D. discoideum</em> to examine the effect of <em>mfsd8</em>-deficiency on the secretome during the early stages of multicellular development. Mass spectrometry revealed 61 proteins that were differentially released by cells after 4 and 8 h of starvation. Most proteins were present in increased amounts in <em>mfsd8</em>^<em>-</em> conditioned buffer compared to WT indicating that loss of <em>mfsd8</em> deregulates protein secretion and/or causes the release of proteins not normally secreted by WT cells. GO term enrichment analyses showed that many of the proteins aberrantly released by <em>mfsd8</em>^<em>-</em> cells localize to compartments and regions of the cell associated with the endo-lysosomal and secretory pathways. Mass spectrometry also revealed proteins previously known to be impacted by the loss of <em>mfsd8</em> (e.g., cathepsin D), as well as proteins that may underlie <em>mfsd8</em>-deficiency phenotypes during aggregation. Finally, we show that <em>mfsd8</em>-deficiency reduces intracellular proteasome 20S activity due to the abnormal release of at least one proteasomal subunit. Together, this study reveals the impact of <em>mfsd8</em> loss on the secretome during <em>D. discoideum</em> aggregation and lays the foundation for follow up work that investigates the role of altered protein release in CLN7 disease.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151361"},"PeriodicalIF":6.6,"publicationDate":"2023-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41106426","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}

{"title":"N-glycosylation at N57/100/110 affects CD44s localization, function and stability in hepatocellular carcinoma","authors":"Qixiang Cheng ,&nbsp;Xibo Hu ,&nbsp;Xiaoqing Zhang ,&nbsp;Depeng Yang ,&nbsp;Guiping Zhao ,&nbsp;Liping Sun ,&nbsp;Meiyi Jiang ,&nbsp;Lijun Yang ,&nbsp;Jialing Cai ,&nbsp;Bing Wang ,&nbsp;Mengmeng Zhang ,&nbsp;Fang Han ,&nbsp;Yu Li ,&nbsp;Huan Nie","doi":"10.1016/j.ejcb.2023.151360","DOIUrl":"10.1016/j.ejcb.2023.151360","url":null,"abstract":"<div><p>The glycosylation levels of proteins in cancer cells are closely related to cancer invasion and migration. CD44 is a transmembrane glycoprotein that is significantly overexpressed in a variety of tumor cells and has been proven to promote the migration and motility of cancer cells, but the effect of its N-glycosylation modification on CD44 protein function in tumors is less studied. Here, we investigated the effect of six N-glycan chains (N25/57/100/110/120/255) on CD44s localization, function and stability in hepatocarcinoma cells. When the six sites were mutated, we found that CD44s lost its membrane localization in Huh7 and MHCC-97H cells. On this basis, we identified three glycosylation sites on CD44s (N57, N100 and N110) that played key roles in intracellular localization. When N57, N100 and N110 were mutated together, CD44 localized to the cytoplasm, while another three-site mutant (N25/N120/N255) was still anchored to the membrane. In addition, the ability of CD44-N57Q/N100Q/N110Q to promote the metastasis and invasion of Huh7 and 97H cells was weakened compared with that of CD44-N25Q/N120Q/N255Q. Furthermore, CD44-N57Q/N100Q/N110Q accumulated abnormally in the ER, and a high level of the ER stress (ERS) marker BiP was detected at the same time compared with wild-type CD44. When the lysosome inhibitor CQ was added, the content of mutant protein that triggered ERS significantly increased, which indicated that the degradation mode of CD44-N57Q/N100Q/N110Q after ERS was mainly through the lysosomal pathway (ERLAD). The results revealed that the N-glycosylation sites N57, N100 and N110 mutated on CD44s affected its function and degraded it by lysosomes after triggering ERS. These findings provide data for new studies on ER-related degradation, further promote the study of the glycan chain function of CD44 and furnish new ideas for the treatment of liver cancer metastasis.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151360"},"PeriodicalIF":6.6,"publicationDate":"2023-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10222290","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}

{"title":"Regulation of integrin α5β1-mediated Staphylococcus aureus cellular invasion by the septin cytoskeleton","authors":"Stevens Robertin,&nbsp;Dominik Brokatzky,&nbsp;Damián Lobato-Márquez ,&nbsp;Serge Mostowy","doi":"10.1016/j.ejcb.2023.151359","DOIUrl":"10.1016/j.ejcb.2023.151359","url":null,"abstract":"<div><p><em>Staphylococcus aureus</em>, a Gram-positive bacterial pathogen, is an urgent health threat causing a wide range of clinical infections. Originally viewed as a strict extracellular pathogen, accumulating evidence has revealed <em>S. aureus</em> to be a facultative intracellular pathogen subverting host cell signalling to support invasion. The majority of clinical isolates produce fibronectin-binding proteins A and B (FnBPA and FnBPB) to interact with host integrin α5β1, a key component of focal adhesions. <em>S. aureus</em> binding of integrin α5β1 promotes its clustering on the host cell surface, triggering activation of focal adhesion kinase (FAK) and cytoskeleton rearrangements to promote bacterial invasion into non-phagocytic cells. Here, we discover that septins, a component of the cytoskeleton that assembles on membranes, are recruited as collar-like structures with actin to <em>S. aureus</em> invasion sites engaging integrin α5β1. To investigate septin recruitment to the plasma membrane in a bacteria-free system, we used FnBPA-coated latex beads and showed that septins are recruited upon activation of integrin α5β1. SEPT2 depletion reduced <em>S. aureus</em> invasion, but increased surface expression of integrin α5 and adhesion of <em>S. aureus</em> to host cells. Consistent with this, SEPT2 depletion increased cellular protein levels of integrin α5 and β1 subunits, as well as FAK. Collectively, these results provide insights into regulation of integrin α5β1 and invasion of <em>S. aureus</em> by the septin cytoskeleton.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151359"},"PeriodicalIF":6.6,"publicationDate":"2023-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10276324","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}

{"title":"ING1 inhibits Twist1 expression to block EMT and is antagonized by the HDAC inhibitor vorinostat","authors":"Yang Yang ,&nbsp;Biao Ma ,&nbsp;Mahbod Djamshidi ,&nbsp;Qingrun Zhang ,&nbsp;Anusi Sarkar ,&nbsp;Ayan Chanda ,&nbsp;Uyen Tran ,&nbsp;Jung Soh ,&nbsp;Christina Sandall ,&nbsp;Huey-Miin Chen ,&nbsp;Justin A. MacDonald ,&nbsp;Shirin Bonni ,&nbsp;Christoph W. Sensen ,&nbsp;Jianhua Zheng ,&nbsp;Karl Riabowol","doi":"10.1016/j.ejcb.2023.151341","DOIUrl":"10.1016/j.ejcb.2023.151341","url":null,"abstract":"<div><p>ING1 is a chromatin targeting subunit of the Sin3a histone deacetylase (HDAC) complex that alters chromatin structure to subsequently regulate gene expression. We find that ING1 knockdown increases expression of Twist1, Zeb 1&amp;2, Snai1, Bmi1 and TSHZ1 drivers of EMT, promoting EMT and cell motility. ING1 expression had the opposite effect, promoting epithelial cell morphology and inhibiting basal and TGF-β-induced motility in 3D organoid cultures. ING1 binds the Twist1 promoter and Twist1 was largely responsible for the ability of ING1 to reduce cell migration. Consistent with ING1 inhibiting Twist1 expression in vivo, an inverse relationship between ING1 and Twist1 levels was seen in breast cancer samples from The Cancer Genome Atlas (TCGA). The HDAC inhibitor vorinostat is approved for treatment of multiple myeloma and cutaneous T cell lymphoma and is in clinical trials for solid tumours as adjuvant therapy. One molecular target of vorinostat is INhibitor of Growth 2 (ING2), that together with ING1 serve as targeting subunits of the Sin3a HDAC complex. Treatment with sublethal (LD25-LD50) levels of vorinostat promoted breast cancer cell migration several-fold, which increased further upon ING1 knockout. These observations indicate that correct targeting of the Sin3a HDAC complex, and HDAC activity in general decreases luminal and basal breast cancer cell motility, suggesting that use of HDAC inhibitors as adjuvant therapies in breast cancers that are prone to metastasize may not be optimal and requires further investigation.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 3","pages":"Article 151341"},"PeriodicalIF":6.6,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9827137","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}

{"title":"Leptin deficiency impairs adipogenesis and browning response in mouse mesenchymal progenitors","authors":"Ksenija Velickovic ,&nbsp;Hilda Anaid Lugo Leija ,&nbsp;Bojana Kosic ,&nbsp;Harold Sacks ,&nbsp;Michael E. Symonds ,&nbsp;Virginie Sottile","doi":"10.1016/j.ejcb.2023.151342","DOIUrl":"10.1016/j.ejcb.2023.151342","url":null,"abstract":"<div><p>Although phenotypically different, brown adipose tissue (BAT) and inguinal white adipose tissue (iWAT) are able to produce heat through non-shivering thermogenesis due to the presence of mitochondrial uncoupling protein 1 (UCP1). The appearance of thermogenically active beige adipocytes in iWAT is known as browning<em>.</em> Both brown and beige cells originate from mesenchymal stem cells (MSCs), and in culture conditions a browning response can be induced with hypothermia (i.e. 32 °C) during which nuclear leptin immunodetection was observed. The central role of leptin in regulating food intake and energy consumption is well recognised, but its importance in the browning process at the cellular level is unclear. Here, immunocytochemical analysis of MSC-derived adipocytes established nuclear localization of both leptin and leptin receptor suggesting an involvement of the leptin pathway in the browning response. In order to elucidate whether leptin modulates the expression of brown and beige adipocyte markers, BAT and iWAT samples from leptin-deficient (<em>ob/ob</em>) mice were analysed and exhibited reduced brown/beige marker expression compared to wild-type controls. When MSCs were isolated and differentiated into adipocytes, leptin deficiency was observed to induce a white phenotype, especially when incubated at 32 °C. These adaptations were accompanied with morphological signs of impaired adipogenic differentiation. Overall, our results indicate that leptin supports adipocyte browning and suggest a potential role for leptin in adipogenesis and browning.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 3","pages":"Article 151342"},"PeriodicalIF":6.6,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9834710","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}

{"title":"Bone marrow mesenchymal/fibroblastic stromal cells induce a distinctive EMT-like phenotype in AML cells","authors":"N. Nojszewska ,&nbsp;O. Idilli ,&nbsp;D. Sarkar ,&nbsp;Z. Ahouiyek ,&nbsp;Y. Arroyo-Berdugo ,&nbsp;C. Sandoval ,&nbsp;MS Amin-Anjum ,&nbsp;S. Bowers ,&nbsp;D. Greaves ,&nbsp;L. Saeed ,&nbsp;M. Khan ,&nbsp;S. Salti ,&nbsp;S. Al-Shami ,&nbsp;H. Topoglu ,&nbsp;JK Punzalan ,&nbsp;JG Farias ,&nbsp;Y. Calle","doi":"10.1016/j.ejcb.2023.151334","DOIUrl":"10.1016/j.ejcb.2023.151334","url":null,"abstract":"<div><p>The development of epithelial-to-mesenchymal transition (EMT) like features is emerging as a critical factor involved in the pathogenesis of acute myeloid leukaemia (AML). However, the extracellular signals and the signalling pathways in AML that may regulate EMT remain largely unstudied. We found that the bone marrow (BM) mesenchymal/fibroblastic cell line HS5 induces an EMT-like migratory phenotype in AML cells. AML cells underwent a strong increase of vimentin (VIM) levels that was not mirrored to the same extent by changes of expression of the other EMT core proteins SNAI1 and SNAI2. We validated these particular pattern of co-expression of core-EMT markers in AML cells by performing an <em>in silico</em> analysis using datasets of human tumours. Our data showed that in AML the expression levels of <em>VIM</em> does not completely correlate with the co-expression of core EMT markers observed in epithelial tumours. We also found that <em>vs</em> epithelial tumours, AML cells display a distinct patterns of co-expression of <em>VIM</em> and the actin binding and adhesion regulatory proteins that regulate F-actin dynamics and integrin-mediated adhesions involved in the invasive migration in cells undergoing EMT. We conclude that the BM stroma induces an EMT related pattern of migration in AML cells in a process involving a distinctive regulation of EMT markers and of regulators of cell adhesion and actin dynamics that should be further investigated. Understanding the tumour specific signalling pathways associated with the EMT process may contribute to the development of new tailored therapies for AML as well as in different types of cancers.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 3","pages":"Article 151334"},"PeriodicalIF":6.6,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9671800","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}