Nature Cell Biology最新文献_第8页

The stress response regulator HSF1 modulates natural killer cell anti-tumour immunity 应激反应调节因子 HSF1 可调节自然杀伤细胞的抗肿瘤免疫力

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2024-09-02 DOI: 10.1038/s41556-024-01490-z

Kathryn Hockemeyer, Theodore Sakellaropoulos, Xufeng Chen, Olha Ivashkiv, Maria Sirenko, Hua Zhou, Giovanni Gambi, Elena Battistello, Kleopatra Avrampou, Zhengxi Sun, Maria Guillamot, Luis Chiriboga, George Jour, Igor Dolgalev, Kate Corrigan, Kamala Bhatt, Iman Osman, Aristotelis Tsirigos, Nikos Kourtis, Iannis Aifantis

{"title":"The stress response regulator HSF1 modulates natural killer cell anti-tumour immunity","authors":"Kathryn Hockemeyer, Theodore Sakellaropoulos, Xufeng Chen, Olha Ivashkiv, Maria Sirenko, Hua Zhou, Giovanni Gambi, Elena Battistello, Kleopatra Avrampou, Zhengxi Sun, Maria Guillamot, Luis Chiriboga, George Jour, Igor Dolgalev, Kate Corrigan, Kamala Bhatt, Iman Osman, Aristotelis Tsirigos, Nikos Kourtis, Iannis Aifantis","doi":"10.1038/s41556-024-01490-z","DOIUrl":"10.1038/s41556-024-01490-z","url":null,"abstract":"Diverse cellular insults converge on activation of the heat shock factor 1 (HSF1), which regulates the proteotoxic stress response to maintain protein homoeostasis. HSF1 regulates numerous gene programmes beyond the proteotoxic stress response in a cell-type- and context-specific manner to promote malignancy. However, the role(s) of HSF1 in immune populations of the tumour microenvironment remain elusive. Here, we leverage an in vivo model of HSF1 activation and single-cell transcriptomic tumour profiling to show that augmented HSF1 activity in natural killer (NK) cells impairs cytotoxicity, cytokine production and subsequent anti-tumour immunity. Mechanistically, HSF1 directly binds and regulates the expression of key mediators of NK cell effector function. This work demonstrates that HSF1 regulates the immune response under the stress conditions of the tumour microenvironment. These findings have important implications for enhancing the efficacy of adoptive NK cell therapies and for designing combinatorial strategies including modulators of NK cell-mediated tumour killing. Hockemeyer et al. demonstrate that HSF1 activation inhibits cytokine production and cytotoxic activity in NK cells to impair anti-tumour immune responses.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"26 10","pages":"1734-1744"},"PeriodicalIF":17.3,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142118146","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}

引用次数: 0

Criteria for the standardization of stem-cell-based embryo models 干细胞胚胎模型标准化标准

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2024-09-02 DOI: 10.1038/s41556-024-01492-x

Alfonso Martinez Arias, Nicolas Rivron, Naomi Moris, Patrick Tam, Cantas Alev, Jianping Fu, Anna-Katerina Hadjantonakis, Jacob H. Hanna, Gabriella Minchiotti, Olivier Pourquie, Guojun Sheng, Liliana Solnica Krezel, Jesse V. Veenvliet, Aryeh Warmflash

引用次数: 0

LIANA+ provides an all-in-one framework for cell–cell communication inference LIANA+ 为细胞间通信推断提供了一体化框架

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2024-09-02 DOI: 10.1038/s41556-024-01469-w

Daniel Dimitrov, Philipp Sven Lars Schäfer, Elias Farr, Pablo Rodriguez-Mier, Sebastian Lobentanzer, Pau Badia-i-Mompel, Aurelien Dugourd, Jovan Tanevski, Ricardo Omar Ramirez Flores, Julio Saez-Rodriguez

{"title":"LIANA+ provides an all-in-one framework for cell–cell communication inference","authors":"Daniel Dimitrov, Philipp Sven Lars Schäfer, Elias Farr, Pablo Rodriguez-Mier, Sebastian Lobentanzer, Pau Badia-i-Mompel, Aurelien Dugourd, Jovan Tanevski, Ricardo Omar Ramirez Flores, Julio Saez-Rodriguez","doi":"10.1038/s41556-024-01469-w","DOIUrl":"10.1038/s41556-024-01469-w","url":null,"abstract":"The growing availability of single-cell and spatially resolved transcriptomics has led to the development of many approaches to infer cell–cell communication, each capturing only a partial view of the complex landscape of intercellular signalling. Here we present LIANA+, a scalable framework built around a rich knowledge base to decode coordinated inter- and intracellular signalling events from single- and multi-condition datasets in both single-cell and spatially resolved data. By extending and unifying established methodologies, LIANA+ provides a comprehensive set of synergistic components to study cell–cell communication via diverse molecular mediators, including those measured in multi-omics data. LIANA+ is accessible at https://github.com/saezlab/liana-py with extensive vignettes ( https://liana-py.readthedocs.io/ ) and provides an all-in-one solution to intercellular communication inference. Dimitrov et al. present LIANA+, a framework that unifies and extends approaches to study inter- and intracellular signalling from diverse mediators, captured from single-cell, spatially resolved and multi-omics data.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"26 9","pages":"1613-1622"},"PeriodicalIF":17.3,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41556-024-01469-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142117984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Innate immune sensing of cell death in disease and therapeutics 疾病和治疗中的细胞死亡先天免疫感应

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2024-09-02 DOI: 10.1038/s41556-024-01491-y

Si Ming Man, Thirumala-Devi Kanneganti

{"title":"Innate immune sensing of cell death in disease and therapeutics","authors":"Si Ming Man, Thirumala-Devi Kanneganti","doi":"10.1038/s41556-024-01491-y","DOIUrl":"10.1038/s41556-024-01491-y","url":null,"abstract":"Innate immunity, cell death and inflammation underpin many aspects of health and disease. Upon sensing pathogens, pathogen-associated molecular patterns or damage-associated molecular patterns, the innate immune system activates lytic, inflammatory cell death, such as pyroptosis and PANoptosis. These genetically defined, regulated cell death pathways not only contribute to the host defence against infectious disease, but also promote pathological manifestations leading to cancer and inflammatory diseases. Our understanding of the underlying mechanisms has grown rapidly in recent years. However, how dying cells, cell corpses and their liberated cytokines, chemokines and inflammatory signalling molecules are further sensed by innate immune cells, and their contribution to further amplify inflammation, trigger antigen presentation and activate adaptive immunity, is less clear. Here, we discuss how pattern-recognition and PANoptosome sensors in innate immune cells recognize and respond to cell-death signatures. We also highlight molecular targets of the innate immune response for potential therapeutic development. Man and Kanneganti discuss how pattern-recognition sensors in innate immune cells recognize and respond to cell-death signatures, and highlight molecular targets for potential therapeutic development.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"26 9","pages":"1420-1433"},"PeriodicalIF":17.3,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142118147","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}

引用次数: 0

HSF1 renders NK cells too stressed to respond HSF1 使 NK 细胞压力过大，无法做出反应

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2024-09-02 DOI: 10.1038/s41556-024-01472-1

Yael Gruper, Aviad Ben-Shmuel, Ruth Scherz-Shouval

引用次数: 0

Noncanonical inheritance of phenotypic information by protein amyloids 蛋白质淀粉样蛋白对表型信息的非规范遗传

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2024-09-02 DOI: 10.1038/s41556-024-01494-9

Matthew Eroglu, Tanner Zocher, Jacob McAuley, Rachel Webster, Maggie Z. X. Xiao, Bin Yu, Calvin Mok, W. Brent Derry

{"title":"Noncanonical inheritance of phenotypic information by protein amyloids","authors":"Matthew Eroglu, Tanner Zocher, Jacob McAuley, Rachel Webster, Maggie Z. X. Xiao, Bin Yu, Calvin Mok, W. Brent Derry","doi":"10.1038/s41556-024-01494-9","DOIUrl":"10.1038/s41556-024-01494-9","url":null,"abstract":"All known heritable phenotypic information in animals is transmitted by direct inheritance of nucleic acids, their covalent modifications or histone modifications that modulate expression of associated genomic regions. Nonetheless, numerous familial traits and disorders cannot be attributed to known heritable molecular factors. Here we identify amyloid-like protein structures that are stably inherited in wild-type animals and influence traits. Their perturbation by genetic, environmental or pharmacological treatments leads to developmental phenotypes that can be epigenetically passed onto progeny. Injection of amyloids isolated from different phenotypic backgrounds into naive animals recapitulates the associated phenotype in offspring. Genetic and proteomic analyses reveal that the 26S proteasome and its conserved regulators maintain heritable amyloids across generations, which enables proper germ cell sex differentiation. We propose that inheritance of a proteinaceous epigenetic memory coordinates developmental timing and patterning with the environment to confer adaptive fitness. Eroglu et al. describe protein amyloid structures that are stably inherited across generations and transmit epigenetic memory in Caenorhabditis elegans. MSTR protein loss results in a transgenerational feminization phenotype through ectopic GLD-1 expression.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"26 10","pages":"1712-1724"},"PeriodicalIF":17.3,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142118148","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}

引用次数: 0

A phosphorylation-controlled switch confers cell cycle-dependent protein relocalization 磷酸化控制的开关可实现依赖细胞周期的蛋白质重新定位

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2024-08-29 DOI: 10.1038/s41556-024-01495-8

Xiaofu Cao, Shiying Huang, Mateusz M. Wagner, Yuan-Ting Cho, Din-Chi Chiu, Krista M. Wartchow, Artur Lazarian, Laura Beth McIntire, Marcus B. Smolka, Jeremy M. Baskin

{"title":"A phosphorylation-controlled switch confers cell cycle-dependent protein relocalization","authors":"Xiaofu Cao, Shiying Huang, Mateusz M. Wagner, Yuan-Ting Cho, Din-Chi Chiu, Krista M. Wartchow, Artur Lazarian, Laura Beth McIntire, Marcus B. Smolka, Jeremy M. Baskin","doi":"10.1038/s41556-024-01495-8","DOIUrl":"10.1038/s41556-024-01495-8","url":null,"abstract":"Tools for acute manipulation of protein localization enable elucidation of spatiotemporally defined functions, but their reliance on exogenous triggers can interfere with cell physiology. This limitation is particularly apparent for studying mitosis, whose highly choreographed events are sensitive to perturbations. Here we exploit the serendipitous discovery of a phosphorylation-controlled, cell cycle-dependent localization change of the adaptor protein PLEKHA5 to develop a system for mitosis-specific protein recruitment to the plasma membrane that requires no exogenous stimulus. Mitosis-enabled anchor-away/recruiter system comprises an engineered, 15 kDa module derived from PLEKHA5 capable of recruiting functional protein cargoes to the plasma membrane during mitosis, either through direct fusion or via GFP–GFP nanobody interaction. Applications of the mitosis-enabled anchor-away/recruiter system include both knock sideways to rapidly extract proteins from their native localizations during mitosis and conditional recruitment of lipid-metabolizing enzymes for mitosis-selective editing of plasma membrane lipid content, without the need for exogenous triggers or perturbative synchronization methods. Cao et al. describe the development and application of an engineered protein system (MARS) derived from PLEKHA5 that allows mitosis-specific recruitment of proteins to the plasma membrane to study protein function in cell division.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"26 10","pages":"1804-1816"},"PeriodicalIF":17.3,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142090018","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}

引用次数: 0

Nuclear proteasomes buffer cytoplasmic proteins during autophagy compromise 核蛋白酶体在自噬妥协过程中缓冲细胞质蛋白质

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2024-08-29 DOI: 10.1038/s41556-024-01488-7

So Jung Park, Sung Min Son, Antonio Daniel Barbosa, Lidia Wrobel, Eleanna Stamatakou, Ferdinando Squitieri, Gabriel Balmus, David C. Rubinsztein

{"title":"Nuclear proteasomes buffer cytoplasmic proteins during autophagy compromise","authors":"So Jung Park, Sung Min Son, Antonio Daniel Barbosa, Lidia Wrobel, Eleanna Stamatakou, Ferdinando Squitieri, Gabriel Balmus, David C. Rubinsztein","doi":"10.1038/s41556-024-01488-7","DOIUrl":"10.1038/s41556-024-01488-7","url":null,"abstract":"Autophagy is a conserved pathway where cytoplasmic contents are engulfed by autophagosomes, which then fuse with lysosomes enabling their degradation. Mutations in core autophagy genes cause neurological conditions, and autophagy defects are seen in neurodegenerative diseases such as Parkinson’s disease and Huntington’s disease. Thus, we have sought to understand the cellular pathway perturbations that autophagy-perturbed cells are vulnerable to by seeking negative genetic interactions such as synthetic lethality in autophagy-null human cells using available data from yeast screens. These revealed that loss of proteasome and nuclear pore complex components cause synergistic viability changes akin to synthetic fitness loss in autophagy-null cells. This can be attributed to the cytoplasm-to-nuclear transport of proteins during autophagy deficiency and subsequent degradation of these erstwhile cytoplasmic proteins by nuclear proteasomes. As both autophagy and cytoplasm-to-nuclear transport are defective in Huntington’s disease, such cells are more vulnerable to perturbations of proteostasis due to these synthetic interactions. Park et al. show that cells with impaired autophagy shuttle cytoplasmic proteins to the nucleus for degradation by nuclear proteasomes, revealing synergistic vulnerabilities in diseases where autophagy and nucleocytoplasmic transport are compromised.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"26 10","pages":"1691-1699"},"PeriodicalIF":17.3,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41556-024-01488-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142090104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The dual roles of lymphotoxin-β in promoting breast cancer bone metastasis 淋巴毒素-β在促进乳腺癌骨转移中的双重作用

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2024-08-28 DOI: 10.1038/s41556-024-01479-8

引用次数: 0

Single-cell new RNA sequencing reveals principles of transcription at the resolution of individual bursts 单细胞新 RNA 测序揭示了单个突变的转录原理

IF 17.3 1区生物学

Nature Cell Biology Pub Date : 2024-08-28 DOI: 10.1038/s41556-024-01486-9

Daniel Ramsköld, Gert-Jan Hendriks, Anton J. M. Larsson, Juliane V. Mayr, Christoph Ziegenhain, Michael Hagemann-Jensen, Leonard Hartmanis, Rickard Sandberg

{"title":"Single-cell new RNA sequencing reveals principles of transcription at the resolution of individual bursts","authors":"Daniel Ramsköld, Gert-Jan Hendriks, Anton J. M. Larsson, Juliane V. Mayr, Christoph Ziegenhain, Michael Hagemann-Jensen, Leonard Hartmanis, Rickard Sandberg","doi":"10.1038/s41556-024-01486-9","DOIUrl":"10.1038/s41556-024-01486-9","url":null,"abstract":"Analyses of transcriptional bursting from single-cell RNA-sequencing data have revealed patterns of variation and regulation in the kinetic parameters that could be inferred. Here we profiled newly transcribed (4-thiouridine-labelled) RNA across 10,000 individual primary mouse fibroblasts to more broadly infer bursting kinetics and coordination. We demonstrate that inference from new RNA profiles could separate the kinetic parameters that together specify the burst size, and that the synthesis rate (and not the transcriptional off rate) controls the burst size. Importantly, transcriptome-wide inference of transcriptional on and off rates provided conclusive evidence that RNA polymerase II transcribes genes in bursts. Recent reports identified examples of transcriptional co-bursting, yet no global analyses have been performed. The deep new RNA profiles we generated with allelic resolution demonstrated that co-bursting rarely appears more frequently than expected by chance, except for certain gene pairs, notably paralogues located in close genomic proximity. Altogether, new RNA single-cell profiling critically improves the inference of transcriptional bursting and provides strong evidence for independent transcriptional bursting of mammalian genes. Ramskold, Hendriks, Larsson et al. use deep single-cell profiling of newly transcribed RNA to uncover the kinetics and dynamics of transcriptional bursting at allelic resolution in primary mouse cells.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"26 10","pages":"1725-1733"},"PeriodicalIF":17.3,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41556-024-01486-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142084967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0