European journal of cell biology最新文献

{"title":"Rel governs loser elimination during stem cell competition in the Drosophila testis","authors":"Silvana Hof-Michel ,&nbsp;Ljubinka Cigoja ,&nbsp;Sabina Huhn ,&nbsp;Christian Bökel","doi":"10.1016/j.ejcb.2023.151375","DOIUrl":"10.1016/j.ejcb.2023.151375","url":null,"abstract":"<div><p>In the <em>Drosophila</em> testis, a group of stromal cells termed hub provides multiple niche signals for the surrounding germline and somatic stem cells. Stem cells of both populations compete for physical retention in the niche, and clones unable to transduce any one niche signal are rapidly eliminated from the stem cell pool by differentiation. We have mapped the transcriptomes of isolated somatic cyst stem cells and differentiated cyst cells, and found that the stem cells but not their differentiated progeny exhibit the signature of an innate immune response including the NF-κB transcription factor Relish (Rel). Related signalling pathways had previously implicated in cell competition in larval epithelia, prompting the question of whether NF-κB signalling was, despite the clear differences between the two competition scenarios, also involved in stem cell competition in the testis. Here we show i) that in the testis Rel is dispensable for stemness, ii) that loss of Rel or the upstream receptor Toll suppresses loser elimination following a variety of different triggers used to induce loser fate, and iii) that clonal Rel activation is sufficient for the displacement of neutral or winner cells from the niche, even if these cells otherwise retain stem cell properties.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"103 1","pages":"Article 151375"},"PeriodicalIF":6.6,"publicationDate":"2023-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933523000900/pdfft?md5=769249e9da210b6c07c5b0ff2695bf6b&pid=1-s2.0-S0171933523000900-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138298780","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}

{"title":"Extracellular vesicles on the move: Traversing the complex matrix of tissues","authors":"Syrine Arif ,&nbsp;Véronique J. Moulin","doi":"10.1016/j.ejcb.2023.151372","DOIUrl":"https://doi.org/10.1016/j.ejcb.2023.151372","url":null,"abstract":"<div><p>Extracellular vesicles are small particles involved in intercellular signaling. They are produced by virtually all cell types, transport biological molecules, and are released into the extracellular space. Studies on extracellular vesicles have become more numerous in recent years, leading to promising research on their potential impact on health and disease. Despite significant progress in understanding the bioactivity of extracellular vesicles, most in vitro and in vivo studies overlook their transport through the extracellular matrix in tissues. The interaction or free diffusion of extracellular vesicles in their environment can provide valuable insights into their efficacy and function. Therefore, understanding the factors that influence the transport of extracellular vesicles in the extracellular matrix is essential for the development of new therapeutic approaches that involve the use of these extracellular vesicles. This review discusses the importance of the interaction between extracellular vesicles and the extracellular matrix and the different factors that influence their diffusion. In addition, we evaluate their role in tissue homeostasis, pathophysiology, and potential clinical applications. Understanding the complex interaction between extracellular vesicles and the extracellular matrix is critical in order to develop effective strategies to target specific cells and tissues in a wide range of clinical applications.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151372"},"PeriodicalIF":6.6,"publicationDate":"2023-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933523000870/pdfft?md5=a815314c8d69ffea1008a56b8d41fca1&pid=1-s2.0-S0171933523000870-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134653311","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}

{"title":"MitoTracker: A useful tool in need of better alternatives","authors":"Kit Neikirk ,&nbsp;Andrea G. Marshall ,&nbsp;Bartosz Kula ,&nbsp;Nathan Smith ,&nbsp;Sharonda LeBlanc ,&nbsp;Antentor Hinton Jr.","doi":"10.1016/j.ejcb.2023.151371","DOIUrl":"https://doi.org/10.1016/j.ejcb.2023.151371","url":null,"abstract":"<div><p>The fluorescence viewing of mitochondria is commonly performed by MitoTracker, a lipophilic cationic dye that is taken up by the mitochondria. In this forum, we highlight several issues that may occur with MitoTracker, including staining of other organelles. Our aim is to offer alternative dyes and discuss their advantages and disadvantages. We also offer options for software with alternatives to MitoTracker to expedite future experimental design.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151371"},"PeriodicalIF":6.6,"publicationDate":"2023-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933523000869/pdfft?md5=9053b4c8a6812de3e6dcae0de67d220d&pid=1-s2.0-S0171933523000869-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91989550","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}

{"title":"Modelling Legionnaires’ disease: Lessons learned from invertebrate and vertebrate animal models","authors":"Clarisse Leseigneur,&nbsp;Carmen Buchrieser","doi":"10.1016/j.ejcb.2023.151369","DOIUrl":"10.1016/j.ejcb.2023.151369","url":null,"abstract":"<div><p>The study of virulence of <em>Legionella pneumophila</em> and its interactions with its hosts has been predominantly conducted <em>in cellulo</em> in the past decades. Although easy to implement and allowing the dissection of molecular pathways underlying host-pathogen interactions, these cellular models fail to provide conditions of the complex environments encountered by the bacteria during the infection of multicellular organisms. To improve our understanding of human infection, several animal models have been developed. This review provides an overview of the invertebrate and vertebrate models that have been established to study <em>L. pneumophila</em> infection and that are alternatives to the classical mouse model, which does not recall human infection with <em>L. pneumophila</em> well. Finally we provide insight in the main contributions made by these models along with their pros and cons.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151369"},"PeriodicalIF":6.6,"publicationDate":"2023-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933523000845/pdfft?md5=1baed8f7d946572b025dabfa2bde80f7&pid=1-s2.0-S0171933523000845-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71479677","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}

{"title":"Reconstitution of actin-based cellular processes: Why encapsulation changes the rules","authors":"Fabina Binth Kandiyoth,&nbsp;Alphée Michelot","doi":"10.1016/j.ejcb.2023.151368","DOIUrl":"10.1016/j.ejcb.2023.151368","url":null,"abstract":"<div><p>While in vitro reconstitution of cellular processes is progressing rapidly, the encapsulation of biomimetic systems to reproduce the cellular environment is a major challenge. Here we review the difficulties, using reconstitution of processes dependent on actin polymerization as an example. Some of the problems are purely technical, due to the need for engineering strategies to encapsulate concentrated solutions in micrometer-sized compartments. However, other significant issues arise from the reduction of experimental volumes, which alters the chemical evolution of these non-equilibrium systems. Important parameters to consider for successful reconstitutions are the amount of each component, their consumption and renewal rates to guarantee their continuous availability.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151368"},"PeriodicalIF":6.6,"publicationDate":"2023-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933523000833/pdfft?md5=26846c3acaf5ad92219684f45c0a8f3a&pid=1-s2.0-S0171933523000833-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71479678","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}

{"title":"Beyond uniformity: Exploring the heterogeneous and dynamic nature of the microtubule lattice","authors":"Mariana Romeiro Motta ,&nbsp;Subham Biswas ,&nbsp;Laura Schaedel","doi":"10.1016/j.ejcb.2023.151370","DOIUrl":"10.1016/j.ejcb.2023.151370","url":null,"abstract":"<div><p>A fair amount of research on microtubules since their discovery in 1963 has focused on their dynamic tips. In contrast, the microtubule lattice was long believed to be highly regular and static, and consequently received far less attention. Yet, as it turned out, the microtubule lattice is neither as regular, nor as static as previously believed: structural studies uncovered the remarkable wealth of different conformations the lattice can accommodate. In the last decade, the microtubule lattice was shown to be labile and to spontaneously undergo renovation, a phenomenon that is intimately linked to structural defects and was called “microtubule self-repair\". Following this breakthrough discovery, further recent research provided a deeper understanding of the lattice self-repair mechanism, which we review here. Instrumental to these discoveries were <em>in vitro</em> microtubule reconstitution assays, in which microtubules are grown from the minimal components required for their dynamics. In this review, we propose a shift from the term “lattice self-repair” to “lattice dynamics”, since this phenomenon is an inherent property of microtubules and can happen without microtubule damage. We focus on how <em>in vitro</em> microtubule reconstitution assays helped us learn (1) which types of structural variations microtubules display, (2) how these structural variations influence lattice dynamics and microtubule damage caused by mechanical stress, (3) how lattice dynamics impact tip dynamics, and (4) how microtubule-associated proteins (MAPs) can play a role in structuring the lattice. Finally, we discuss the unanswered questions about lattice dynamics and how technical advances will help us tackle these questions.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151370"},"PeriodicalIF":6.6,"publicationDate":"2023-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933523000857/pdfft?md5=5fd74ab2e654cc086a54e91205f41801&pid=1-s2.0-S0171933523000857-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71479676","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}

{"title":"Reconstitution of the transition from a lamellipodia- to filopodia-like actin network with purified proteins","authors":"Cristian Suarez ,&nbsp;Jonathan D. Winkelman ,&nbsp;Alyssa J. Harker ,&nbsp;Hannah J. Ye ,&nbsp;Patrick M. McCall ,&nbsp;Alisha N. Morganthaler ,&nbsp;Margaret L. Gardel ,&nbsp;David R. Kovar","doi":"10.1016/j.ejcb.2023.151367","DOIUrl":"10.1016/j.ejcb.2023.151367","url":null,"abstract":"<div><p>How cells utilize complex mixtures of actin binding proteins to assemble and maintain functionally diverse actin filament networks with distinct architectures and dynamics within a common cytoplasm is a longstanding question in cell biology. A compelling example of complex and specialized actin structures in cells are filopodia which sense extracellular chemical and mechanical signals to help steer motile cells. Filopodia have distinct actin architecture, composed of long, parallel actin filaments bundled by fascin, which form finger-like membrane protrusions. Elongation of the parallel actin filaments in filopodia can be mediated by two processive actin filament elongation factors, formin and Ena/VASP, which localize to the tips of filopodia. There remains debate as to how the architecture of filopodia are generated, with one hypothesis proposing that filopodia are generated from the lamellipodia, which consists of densely packed, branched actin filaments nucleated by Arp2/3 complex and kept short by capping protein. It remains unclear if different actin filament elongation factors are necessary and sufficient to facilitate the emergence of filopodia with diverse characteristics from a highly dense network of short-branched capped filaments. To address this question, we combined bead motility and micropatterning biomimetic assays with multi-color Total Internal Reflection Fluorescence microscopy imaging, to successfully reconstitute the formation of filopodia-like networks (FLN) from densely-branched lamellipodia-like networks (LLN) with eight purified proteins (actin, profilin, Arp2/3 complex, Wasp pWA, fascin, capping protein, VASP and formin mDia2). Saturating capping protein concentrations inhibit FLN assembly, but the addition of either formin or Ena/VASP differentially rescues the formation of FLN from LLN. Specifically, we found that formin/mDia2-generated FLNs are relatively long and lack capping protein, whereas VASP-generated FLNs are comparatively short and contain capping protein, indicating that the actin elongation factor can affect the architecture and composition of FLN emerging from LLN. Our biomimetic reconstitution systems reveal that formin or VASP are necessary and sufficient to induce the transition from a LLN to a FLN, and establish robust in vitro platforms to investigate FLN assembly mechanisms.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151367"},"PeriodicalIF":6.6,"publicationDate":"2023-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0171933523000821/pdfft?md5=6a99bbcd2270f18ccb094c1286e9b991&pid=1-s2.0-S0171933523000821-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61561744","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}

{"title":"Microtubule rescue control by drugs and MAPs examined with in vitro pedestal assay","authors":"Mikhail N. Anisimov ,&nbsp;Alena V. Korshunova ,&nbsp;Vladimir V. Popov ,&nbsp;Nikita B. Gudimchuk","doi":"10.1016/j.ejcb.2023.151366","DOIUrl":"10.1016/j.ejcb.2023.151366","url":null,"abstract":"<div><p>Microtubules are essential cytoskeletal polymers, which exhibit stochastic transitions between assembly and disassembly, known as catastrophes and rescues. Understanding of catastrophes, rescues, and their control by drugs and microtubule associated proteins (MAPs) has been informed by <em>in vitro</em> reconstitutions of microtubule dynamics. In such experiments microtubules are typically observed on a flat surface of the coverslip. In contrast, we have recently proposed a modified setup in which microtubules assemble from stabilized seeds, overhanging from microfabricated pedestals, so that their dynamic extensions are fully isolated from contact with the coverslip. This assay allows to eliminate potential artifacts, which may substantially affect the frequency of microtubule rescues <em>in vitro</em>. Here we use the pedestal assay to study the sensitivity of microtubules to paclitaxel, one of the best-known inhibitors of microtubule dynamics. By comparing observations in the conventional and the pedestal assays, we find that microtubule dynamics are substantially more sensitive to paclitaxel when the polymers can contact the coverslip. We interpret this as a consequence of the coverslip-induced microtubule assembly perturbation, leading to formation of lattice with defects, and thereby enhancing the efficiency of paclitaxel binding to microtubules in the conventional assay. To test this idea, we use vinblastine, another small-molecule inhibitor, which had been previously shown to cause microtubule growth perturbations. We find that in the pedestal assay vinblastine sensitizes microtubules to paclitaxel to the level, observed in the conventional assay. Interestingly, a minimal fragment of MAP called CLASP2, a previously characterized rescue factor, has a strong effect on microtubule rescues, regardless of the type of assay. Overall, our study underscores the role of microtubule damage in promoting rescues and highlights the utility of the <em>in vitro</em> pedestal assay to study microtubule dynamics modulation by tubulin inhibitors and MAPs.</p></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"102 4","pages":"Article 151366"},"PeriodicalIF":6.6,"publicationDate":"2023-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49689424","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":"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}