Biology of the Cell最新文献

{"title":"Role of regulatory C-terminal motifs in synaptic confinement of LRRTM2","authors":"Konstantina Liouta,&nbsp;Julia Chabbert,&nbsp;Sebastien Benquet,&nbsp;Béatrice Tessier,&nbsp;Vincent Studer,&nbsp;Matthieu Sainlos,&nbsp;Joris De Wit,&nbsp;Olivier Thoumine,&nbsp;Ingrid Chamma","doi":"10.1111/boc.202100026","DOIUrl":"10.1111/boc.202100026","url":null,"abstract":"<p>Leucine Rich Repeat Transmembrane proteins (LRRTMs) are neuronal cell adhesion molecules involved in synapse development and plasticity. LRRTM2 is the most synaptogenic isoform of the family, and its expression is strongly restricted to excitatory synapses in mature neurons. However, the mechanisms by which LRRTM2 is trafficked and stabilized at synapses remain unknown. Here, we examine the role of LRRTM2 intracellular domain on its membrane expression and stabilization at excitatory synapses, using a knock-down strategy combined to single molecule tracking and super-resolution dSTORM microscopy. We show that LRRTM2 operates an important shift in mobility after synaptogenesis in hippocampal neurons. Knock-down of LRRTM2 during synapse formation reduced excitatory synapse density in mature neurons. Deletion of LRRTM2 C-terminal domain abolished the compartmentalization of LRRTM2 in dendrites and disrupted its synaptic enrichment. Furtheremore, we show that LRRTM2 diffusion is increased in the absence of its intracellular domain, and that the protein is more dispersed at synapses. Surprisingly, LRRTM2 confinement at synapses was strongly dependent on a YxxC motif in the C-terminal domain, but was independent of the PDZ-like binding motif ECEV. Finally, the nanoscale organization of LRRTM2 at excitatory synapses depended on its C-terminal domain, with involvement of both the PDZ-binding and YxxC motifs. Altogether, these results demonstrate that LRRTM2 trafficking and enrichment at excitatory synapses are dependent on its intracellular domain.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"113 12","pages":"492-506"},"PeriodicalIF":2.7,"publicationDate":"2021-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/boc.202100026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39415695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantitative dSTORM super-resolution microscopy localizes Aurora kinase A/AURKA in the mitochondrial matrix","authors":"Béatrice Durel,&nbsp;Charles Kervrann,&nbsp;Giulia Bertolin","doi":"10.1111/boc.202100021","DOIUrl":"10.1111/boc.202100021","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background information</h3>\u0000 \u0000 <p>Mitochondria are dynamic organelles playing essential metabolic and signaling functions in cells. Their ultrastructure has largely been investigated with electron microscopy (EM) techniques. However, quantifying protein-protein proximities using EM is extremely challenging. Super-resolution microscopy techniques as direct stochastic optical reconstruction microscopy (dSTORM) now provide a fluorescent-based, quantitative alternative to EM. Recently, super-resolution microscopy approaches including dSTORM led to valuable advances in our knowledge of mitochondrial ultrastructure, and in linking it with new insights in organelle functions. Nevertheless, dSTORM is mostly used to image integral mitochondrial proteins, and there is little or no information on proteins transiently present at this compartment. The cancer-related Aurora kinase A/AURKA is a protein localized at various subcellular locations, including mitochondria.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We first demonstrate that dSTORM coupled to GcoPS can resolve protein proximities within individual submitochondrial compartments. Then, we show that dSTORM provides sufficient spatial resolution to visualize and quantify the most abundant pool of endogenous AURKA in the mitochondrial matrix, as previously shown for overexpressed AURKA. In addition, we uncover a smaller pool of AURKA localized at the OMM, which could have a potential functional readout. We conclude by demonstrating that aldehyde-based fixatives are more specific for the OMM pool of the kinase instead.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our results indicate that dSTORM coupled to GcoPS colocalization analysis is a suitable approach to explore the compartmentalization of non-integral mitochondrial proteins as AURKA, in a qualitative and quantitative manner. This method also opens up the possibility of analyzing the proximity between AURKA and its multiple mitochondrial partners with exquisite spatial resolution, thereby allowing novel insights into the mitochondrial functions controlled by AURKA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Significance</h3>\u0000 \u0000 <p>Probing and quantifying the presence of endogenous AURKA – a cell cycle-related protein localized at mitochondria – in the different organelle subcompartments, using quantitative dSTORM super-resolution microscopy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"113 11","pages":"458-473"},"PeriodicalIF":2.7,"publicationDate":"2021-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/boc.202100021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39370727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apoptosis induction by the stem cell factor LIN28A","authors":"Yael Attali-Padael,&nbsp;Leah Armon,&nbsp;Achia Urbach","doi":"10.1111/boc.202100011","DOIUrl":"10.1111/boc.202100011","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background information</h3>\u0000 \u0000 <p>Lin28A and its paralog Lin28B are RNA binding proteins expressed in stem and progenitor cells, regulating the balance between their proliferation and differentiation. <i>In-vivo</i> and <i>in-vitro</i> experiments have shown that overexpression of these genes leads to abnormal cell proliferation, which results in many cases in cell transformation and tumor formation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Here we show, for the first time, that Lin28A overexpression can also lead to the opposite effect, i.e. apoptosis induction. We further demonstrate that this effect is specific to Lin28A but not to Lin28B and that it is mediated via the Let-7 independent pathway in a complex mechanism that involves at least several proteins.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions and Significance</h3>\u0000 \u0000 <p>This unexpected observation suggests that cell fate regulation by Lin28 is dependent on a specific cellular/genetic context. Unraveling the cellular and molecular mechanisms underlying this Lin28A overexpression effect may pave the way for novel tumor therapeutic strategies, as Lin28 is commonly expressed in many types of tumors but not in most normal adult cells.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"113 11","pages":"450-457"},"PeriodicalIF":2.7,"publicationDate":"2021-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39347610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Issue Information","authors":"","doi":"10.1111/boc.202170012","DOIUrl":"https://doi.org/10.1111/boc.202170012","url":null,"abstract":"","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/boc.202170012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42865486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The NANOTUMOR consortium - Towards the Tumor Cell Atlas.","authors":"Florent Colin,&nbsp;Kristine Schauer,&nbsp;Ali Hamiche,&nbsp;Pierre Martineau,&nbsp;Jean-Paul Borg,&nbsp;Jan Bednar,&nbsp;Giulia Bertolin,&nbsp;Luc Camoin,&nbsp;Yves Collette,&nbsp;Stephan Dimitrov,&nbsp;Isabelle Fournier,&nbsp;Vincent Hyenne,&nbsp;Marco A Mendoza-Parra,&nbsp;Xavier Morelli,&nbsp;Philippe Rondé,&nbsp;Izabela Sumara,&nbsp;Marc Tramier,&nbsp;Patrick Schultz,&nbsp;Jacky G Goetz","doi":"10.1111/boc.202000135","DOIUrl":"https://doi.org/10.1111/boc.202000135","url":null,"abstract":"<p><p>Cancer is a multi-step disease where an initial tumour progresses through critical steps shaping, in most cases, life-threatening secondary foci called metastases. The oncogenic cascade involves genetic, epigenetic, signalling pathways, intracellular trafficking and/or metabolic alterations within cancer cells. In addition, pre-malignant and malignant cells orchestrate complex and dynamic interactions with non-malignant cells and acellular matricial components or secreted factors within the tumour microenvironment that is instrumental in the progression of the disease. As our aptitude to effectively treat cancer mostly depends on our ability to decipher, properly diagnose and impede cancer progression and metastasis formation, full characterisation of molecular complexes and cellular processes at play along the metastasis cascade is crucial. For many years, the scientific community lacked adapted imaging and molecular technologies to accurately dissect, at the highest resolution possible, tumour and stromal cells behaviour within their natural microenvironment. In that context, the NANOTUMOR consortium is a French national multi-disciplinary workforce which aims at a providing a multi-scale characterisation of the oncogenic cascade, from the atomic level to the dynamic organisation of the cell in response to genetic mutations, environmental changes or epigenetic modifications. Ultimately, this program aims at identifying new therapeutic targets using innovative drug design.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"113 6","pages":"272-280"},"PeriodicalIF":2.7,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/boc.202000135","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25343008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intracellular host cell membrane remodelling induced by SARS-CoV-2 infection in vitro.","authors":"Lucio Ayres Caldas,&nbsp;Fabiana Avila Carneiro,&nbsp;Fabio Luis Monteiro,&nbsp;Ingrid Augusto,&nbsp;Luiza Mendonça Higa,&nbsp;Kildare Miranda,&nbsp;Amilcar Tanuri,&nbsp;Wanderley de Souza","doi":"10.1111/boc.202000146","DOIUrl":"https://doi.org/10.1111/boc.202000146","url":null,"abstract":"<p><strong>Background information: </strong>Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection induces an alteration in the endomembrane system of the mammalian cells. In this study, we used transmission electron microscopy and electron tomography to investigate the main structural alterations in the cytoplasm of Vero cells infected with a SARS-CoV-2 isolate from São Paulo state (Brazil).</p><p><strong>Results: </strong>Different membranous structures derived from the zippered endoplasmic reticulum were observed along with virus assembly through membrane budding. Also, we demonstrated the occurrence of annulate lamellae in the cytoplasm of infected cells and the presence of virus particles in the perinuclear space.</p><p><strong>Conclusions and significance: </strong>This study contributes to a better understanding of the cell biology of SARS-CoV-2 and the mechanisms of the interaction of the virus with the host cell that promote morphological changes, recruitment of organelles and cell components, in a context of a virus-induced membrane remodelling.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"113 6","pages":"281-293"},"PeriodicalIF":2.7,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/boc.202000146","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25379947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial.","authors":"Julien Husson","doi":"10.1111/boc.202100028","DOIUrl":"https://doi.org/10.1111/boc.202100028","url":null,"abstract":"Mechanobiology is an emerging field at the crossroads between biology, physics, mechanics, bioengineering and materials science. It investigates how mechanics can influence cell function: how cells sense and respond to external mechanical properties and forces, and how they generate forces and adapt their mechanical properties to perform functions as varied as adhesion, migration, differentiation or immune response, to name a few. A growing interest for this field is establishing a corpus of evidence suggesting that potentially any cell, of any type, can sense mechanical inputs from its environment and adapt to them. A new horizon opens up for a more comprehensive description of biological processes that includes their mechanical component. Furthermore, because external mechanical cues are involved in many pathological contexts, understanding the interplay between mechanical inputs and cell response should bring new insights into many pathologies, including cancer, atherosclerosis or evasion from immune response. This themed issue on mechanobiology covers a variety of topics at the cellular and subcellular scale. Three contributions focus on immune cells. Since pioneering studies on the biophysics of leukocytes done decades ago, a growing corpus of knowledge has been accumulated on some myeloid cells such as neutrophils. However, surprising discoveries about these foot soldiers of innate immunity are yet to come, including the way they move to explore their environment. In this issue, Garcia-Seyda et al. (2021) lead the way by showing that neutrophils can swim to reach and phagocyte their target. Mechanics of myeloid cells other than neutrophils remain to be fully explored, and Bashant et al. (2020) review how mechanical properties of myeloid cells can be quantified using recently developed high-throughput deformability cytometry. The authors review how these mechanical properties can be influenced by several factors including: differentiation, priming by cytokines and other soluble molecules or mechanical stimulation, disease and pharmacological treatment. On another front of immunobiophysics, T cells attract a lot of attention given their central role in adaptive immunity and recent revolutions in cancer immunotherapy. T cells use a complex recognition machinery to identify presented antigens. This recognition is known to be mechanosensitive, but understanding the details of this process remains the focus of active work. Before forming a synapse, T cells need to arrest on an antigen-presenting cell (APC), which is yet another process where mechanics play a role. Chabaud et al. (2020) review how mechanical forces generated at the T cell–APC interface and beard by specific bonds between T cell receptors and antigens, and adhesive bonds, regulate the arrest of T cells. This themed issue goes also subcellular with the contribution of Allard et al. (2021), which describes how the shape of membrane tubules can be remodelled by the actin cytoskeleton.","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"113 6","pages":"271"},"PeriodicalIF":2.7,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/boc.202100028","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38973483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of ligand endocytosis in notch signalling","authors":"Ekaterina Seib,&nbsp;Thomas Klein","doi":"10.1111/boc.202100009","DOIUrl":"10.1111/boc.202100009","url":null,"abstract":"<p>The Notch signalling receptor is a mechanoreceptor that is activated by force. This force elicits a conformational change in Notch that results in the release of its intracellular domain into the cytosol by two consecutive proteolytic cleavages. In most cases, the force is generated by pulling of the ligands on the receptor upon their endocytosis. In this review, we summarise recent work that shed a more detailed light on the role of endocytosis during ligand-dependent Notch activation and discuss the role of ubiquitylation of the ligands during this process.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"113 10","pages":"401-418"},"PeriodicalIF":2.7,"publicationDate":"2021-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/boc.202100009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39034597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The neuronal ceroid lipofuscinosis-related protein CLN8 regulates endo-lysosomal dynamics and dendritic morphology","authors":"Favio Pesaola,&nbsp;Gonzalo Quassollo,&nbsp;Ana Clara Venier,&nbsp;Ana Lucía De Paul,&nbsp;Ines Noher,&nbsp;Mariano Bisbal","doi":"10.1111/boc.202000016","DOIUrl":"10.1111/boc.202000016","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background Information</h3>\u0000 \u0000 <p>The endo-lysosomal system (ELS) comprises a set of membranous organelles responsible for transporting intracellular and extracellular components within cells. Defects in lysosomal proteins usually affect a large variety of processes and underlie many diseases, most of them with a strong neuronal impact. Mutations in the endoplasmic reticulum-resident CLN8 protein cause CLN8 disease. This condition is one of the 14 known neuronal ceroid lipofuscinoses (NCLs), a group of inherited diseases characterised by accumulation of lipofuscin-like pigments within lysosomes. Besides mediating the transport of soluble lysosomal proteins, recent research suggested a role for CLN8 in the transport of vesicles and lipids, and autophagy. However, the consequences of CLN8 deficiency on ELS structure and activity, as well as the potential impact on neuronal development, remain poorly characterised. Therefore, we performed CLN8 knockdown in neuronal and non-neuronal cell models to analyse structural, dynamic and functional changes in the ELS and to assess the impact of CLN8 deficiency on axodendritic development.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>CLN8 knockdown increased the size of the Golgi apparatus, the number of mobile vesicles and the speed of endo-lysosomes. Using the fluorescent fusion protein mApple-LAMP1-pHluorin, we detected significant lysosomal alkalisation in CLN8-deficient cells. In turn, experiments in primary rat hippocampal neurons showed that CLN8 deficiency decreased the complexity and size of the somatodendritic compartment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our results suggest the participation of CLN8 in vesicular distribution, lysosomal pH and normal development of the dendritic tree. We speculate that the defects triggered by CLN8 deficiency on ELS structure and dynamics underlie morphological alterations in neurons, which ultimately lead to the characteristic neurodegeneration observed in this NCL.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Significance</h3>\u0000 \u0000 <p>This is, to our knowledge, the first characterisation of the effects of CLN8 dysfunction on the structure and dynamics of the ELS. Moreover, our findings suggest a novel role for CLN8 in somatodendritic development, which may account at least in part for the neuropathological manifestations associated with CLN8 disease.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"113 10","pages":"419-437"},"PeriodicalIF":2.7,"publicationDate":"2021-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/boc.202000016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39007794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial protein import as a quality control sensor","authors":"Sebabrata Maity,&nbsp;Oishee Chakrabarti","doi":"10.1111/boc.202100002","DOIUrl":"10.1111/boc.202100002","url":null,"abstract":"<p>Mitochondria are organelles involved in various functions related to cellular metabolism and homoeostasis. Though mitochondria contain own genome, their nuclear counterparts encode most of the different mitochondrial proteins. These are synthesised as precursors in the cytosol and have to be delivered into the mitochondria. These organelles hence have elaborate machineries for the import of precursor proteins from cytosol. The protein import machineries present in both mitochondrial membrane and aqueous compartments show great variability in pre-protein recognition, translocation and sorting across or into it. Mitochondrial protein import machineries also interact transiently with other protein complexes of the respiratory chain or those involved in the maintenance of membrane architecture. Hence mitochondrial protein translocation is an indispensable part of the regulatory network that maintains protein biogenesis, bioenergetics, membrane dynamics and quality control of the organelle. Various stress conditions and diseases that are associated with mitochondrial import defects lead to changes in cellular transcriptomic and proteomic profiles. Dysfunction in mitochondrial protein import also causes over-accumulation of precursor proteins and their aggregation in the cytosol. Multiple pathways may be activated for buffering these harmful consequences. Here, we present a comprehensive picture of import machinery and its role in cellular quality control in response to defective mitochondrial import. We also discuss the pathological consequences of dysfunctional mitochondrial protein import in neurodegeneration and cancer.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"113 9","pages":"375-400"},"PeriodicalIF":2.7,"publicationDate":"2021-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/boc.202100002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38887278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}