Nature Cell Biology最新文献_第5页

A mechanical origin for pregnancy loss related to maternal age 与母亲年龄有关的流产的机械原因。

IF 22.7 1区生物学

Nature Cell Biology Pub Date : 2026-08-27 DOI: 10.1038/s41556-026-02054-z

引用次数: 0

The proportional scaling of mRNA and ribosome concentrations controls eukaryotic cell growth mRNA和核糖体浓度的比例调节控制着真核细胞的生长。

IF 22.7 1区生物学

Nature Cell Biology Pub Date : 2026-08-25 DOI: 10.1038/s41556-026-02045-0

Xin Gao, Michael Lanz, Rosslyn Grosely, Jonas Cremer, Joseph Puglisi, Jan M. Skotheim

{"title":"The proportional scaling of mRNA and ribosome concentrations controls eukaryotic cell growth","authors":"Xin Gao, Michael Lanz, Rosslyn Grosely, Jonas Cremer, Joseph Puglisi, Jan M. Skotheim","doi":"10.1038/s41556-026-02045-0","DOIUrl":"10.1038/s41556-026-02045-0","url":null,"abstract":"Cell growth underlies nearly all eukaryotic physiology, yet its quantitative principles remain unclear. Here, using single-molecule ribosome tracking, spike-in RNA sequencing and quantitative proteomics across 15 nutrient-limited conditions in budding yeast, we define how growth is controlled in the budding yeast Saccharomyces cerevisiae. Ribosome concentration scales linearly with growth rate, while peptide elongation speed remains constant at approximately nine amino acids per second. While elongation is not a regulatory lever, total mRNA concentration increases proportionally with ribosomes to accelerate growth. A simple kinetic model of mRNA–ribosome binding accurately predicts the fraction of active ribosomes, growth rate and responses to transcriptional or size perturbations. Consistent with this model, transient inhibition of mRNA degradation boosts growth by elevating mRNA concentration. These results reveal that eukaryotic cells accelerate proliferation primarily by proportionally scaling mRNA and ribosome abundance, establishing a quantitative framework for understanding eukaryotic biosynthesis. Gao et al. show that yeast grow faster by proportionally increasing mRNA and ribosome concentrations to increase actively translating ribosomes, while elongation remains constant. A mass-action model explains growth-rate changes.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"28 9","pages":"1901-1912"},"PeriodicalIF":22.7,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818863","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

Elevated contractility drives implantation failure in mouse embryos from aged females 老年雌性小鼠胚胎收缩力升高导致植入失败。

IF 22.7 1区生物学

Nature Cell Biology Pub Date : 2026-08-25 DOI: 10.1038/s41556-026-02052-1

Kate E. Cavanaugh, M. J. Franco-Oñate, Nicole Horsley, Dilan Gokyer, Tomiris Atazhanova, Diana J. Laird, Patrick W. Oakes, Joan K. Riley, Francesca E. Duncan, MaryEllen Pavone, Matteo Molé, Ricard Alert, Orion D. Weiner

{"title":"Elevated contractility drives implantation failure in mouse embryos from aged females","authors":"Kate E. Cavanaugh, M. J. Franco-Oñate, Nicole Horsley, Dilan Gokyer, Tomiris Atazhanova, Diana J. Laird, Patrick W. Oakes, Joan K. Riley, Francesca E. Duncan, MaryEllen Pavone, Matteo Molé, Ricard Alert, Orion D. Weiner","doi":"10.1038/s41556-026-02052-1","DOIUrl":"10.1038/s41556-026-02052-1","url":null,"abstract":"Women in their mid-30s experience a marked decline in fertility. The origin of these fertility defects resides in the implantation capacity of the embryo itself, but the mechanistic basis of this impairment is not well understood. Here we identify a core mechanical defect in embryos from aged females that impairs their implantation competence. Using mouse models, we find that reproductive ageing drives excessive contractility in the trophectoderm, the outer epithelial lineage that enables implantation. This hypercontractility increases blastocyst tissue surface tension and viscosity, which hinders spreading during implantation. Elevated contractility is both necessary and sufficient for age-associated implantation failure. We identify non-invasive imaging signatures that infer embryo mechanics and predict implantation success for embryos of both young and aged females. Analyses of human embryos and in vitro fertilization clinical datasets reveal conserved age-associated mechanical alterations that correlate with implantation potential. Our work implicates embryo mechanics as a key regulator of reproductive longevity. Cavanaugh et al. show that embryos from aged mice have increased contractility and tissue viscosity on embryonic day 4.5, which leads to poor spreading and attachment. Similar age-associated mechanical changes in human embryos correlate with implantation potential.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"28 9","pages":"1799-1813"},"PeriodicalIF":22.7,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818818","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

DREAMS illuminates spatial DNA and RNA modification landscapes DREAMS照亮了空间DNA和RNA修饰景观。

IF 22.7 1区生物学

Nature Cell Biology Pub Date : 2026-08-24 DOI: 10.1038/s41556-026-02038-z

Yan Peng, Liang Xue, Yujie Zhang, Shuangshuang Feng, Yiting Lu, Houyu Zhang, Mingjie Dong, Chenyang Wang, Meng Bao, Waleed Alam, Yueyang Li, Wuyunhan Ma, Sifei Yu, Lei Zhang, Jie Yin, Jiuming He, Magdalena J. Koziol

{"title":"DREAMS illuminates spatial DNA and RNA modification landscapes","authors":"Yan Peng, Liang Xue, Yujie Zhang, Shuangshuang Feng, Yiting Lu, Houyu Zhang, Mingjie Dong, Chenyang Wang, Meng Bao, Waleed Alam, Yueyang Li, Wuyunhan Ma, Sifei Yu, Lei Zhang, Jie Yin, Jiuming He, Magdalena J. Koziol","doi":"10.1038/s41556-026-02038-z","DOIUrl":"10.1038/s41556-026-02038-z","url":null,"abstract":"DNA and RNA modifications regulate gene expression and RNA processing, but their spatial organization in complex tissues remains elusive. Here we developed DNA RNA Elements Areal Mass Spectrometry (DREAMS), a mass spectrometry imaging platform that spatially maps diverse nucleic acid modifications simultaneously. Applying DREAMS to TET-deficient mouse brains (Tet1Δ/Δ and triple Tet1/2/3Δ/Δ), we uncover TET1’s unexpected role in modulating N1-methyladenosine (m1A), a pivotal RNA modification. While DREAMS reveals broad modification landscapes altered across TET knockouts, we identify TET1-mediated changes in m1A that correlate with transcriptome alterations. Our work establishes DREAMS as a transformative tool for spatial epigenomics/epitranscriptomics and suggests that TET enzymes could influence multiple DNA and RNA modifications with potential gatekeeping roles in nucleic acid regulation. Peng, Xue et al. develop a nucleic acid metabolites detection method, DNA RNA Elements Areal Mass Spectrometry (DREAMS) which enables the identification of DNA and RNA modifications, as well as spatial mapping of these modifications within tissues.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"28 9","pages":"1942-1956"},"PeriodicalIF":22.7,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41556-026-02038-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148813580","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

Circadian control of circulating tumour-derived extracellular vesicle secretion affects targeted therapy efficacy 循环肿瘤来源的细胞外囊泡分泌的昼夜节律控制影响靶向治疗的疗效。

IF 22.7 1区生物学

Nature Cell Biology Pub Date : 2026-08-24 DOI: 10.1038/s41556-026-02047-y

Mingying Chen, Yuqian Zhang, Yiqi Zhu, Jiangxin Hou, Sinong Liu, Qiuyue Wu, Wencheng Wang, Jialu Zhang, Yanling Song

{"title":"Circadian control of circulating tumour-derived extracellular vesicle secretion affects targeted therapy efficacy","authors":"Mingying Chen, Yuqian Zhang, Yiqi Zhu, Jiangxin Hou, Sinong Liu, Qiuyue Wu, Wencheng Wang, Jialu Zhang, Yanling Song","doi":"10.1038/s41556-026-02047-y","DOIUrl":"10.1038/s41556-026-02047-y","url":null,"abstract":"Extracellular vesicles (EVs) are cell-derived nanoparticles that mediate intercellular communication, whereas circulating tumour-derived EVs (ctEVs) promote tumour progression. However, their circadian dynamics remain poorly understood owing to the lack of tools capable of resolving vesicle biogenesis dynamics. Here we introduce ctEV-CLOCK, a strategy enabling 12-h resolution isolation of nascent ctEVs. The method integrates metabolic glycoengineering-based timestamping with tumour-marker-guided selective click tagging, achieving enrichment of ctEV populations within defined time windows. Using this approach, we uncover circadian oscillations in ctEV abundance and functional properties across multiple mouse tumour models. These oscillations are accompanied by time-of-day-dependent alterations in vesicle protein profiles. Importantly, synchronizing targeted therapy with peak ctEV protein abundance markedly enhances therapeutic efficacy. Together, these findings position ctEV circadian dynamics as a regulatory layer in tumour biology and provide a framework for circadian-aligned cancer chronotherapy beyond immune-focused strategies. Chen, Zhang and colleagues report ctEV-CLOCK as a tool to characterize circulating tumour-derived extracellular vesicles and demonstrate a pattern of circadian oscillation, which may be leveraged to design time-synchronized targeted cancer therapy.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"28 9","pages":"1927-1941"},"PeriodicalIF":22.7,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148813624","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

Biosensor reveals unexpected variability in the cGAS response to DNA damage 生物传感器揭示了cGAS对DNA损伤反应的意外变异性。

IF 22.7 1区生物学

Nature Cell Biology Pub Date : 2026-08-21 DOI: 10.1038/s41556-026-02039-y

引用次数: 0

A versatile cGAMP reporter reveals principles of cGAS activation by DNA damage and chromosome instability 一个多功能的cGAMP报告揭示了DNA损伤和染色体不稳定激活cGAS的原理

IF 22.7 1区生物学

Nature Cell Biology Pub Date : 2026-08-21 DOI: 10.1038/s41556-026-02037-0

Vivianne Lebrec, Alexandra Kanellou, Lauren R. Davies, Negar Afshar, Tomoya Kujirai, Robert J. Pickering, Vera Solntceva, Federico Tidu, Christian Zierhut

{"title":"A versatile cGAMP reporter reveals principles of cGAS activation by DNA damage and chromosome instability","authors":"Vivianne Lebrec, Alexandra Kanellou, Lauren R. Davies, Negar Afshar, Tomoya Kujirai, Robert J. Pickering, Vera Solntceva, Federico Tidu, Christian Zierhut","doi":"10.1038/s41556-026-02037-0","DOIUrl":"10.1038/s41556-026-02037-0","url":null,"abstract":"cGAS is the primary innate immune DNA sensor. On binding DNA, cGAS generates cGAMP, ultimately driving inflammation. Although normally silenced on self-DNA, genotoxic stress can activate cGAS, proposed to be mediated by micronuclei, chromosome bridges and DNA:RNA hybrids. However, mechanistically, this is poorly understood due to a lack of sensitive and selective single-cell cGAS activation assays. Here we solve this with an improved cGAMP reporter for microscopy, flow cytometry and biochemical assays. Strikingly, we find that genotoxic stress-mediated cGAS activation is a rare event that is not driven by enrichment on micronuclei and occurs by mechanisms that vary in dependence on the genotoxic stress. Following chromosome mis-segregation, cGAS activation correlates with bridge association but, notably, ionizing radiation activates cGAS independently of bridges. Whereas simple DNA:RNA hybrids are inert, more complex structures such as R-loops activate cGAS. Our work revises the cGAS signalling framework and introduces a flexible tool to examine it. Lebrec et al. present a FRET-based cGAS reporter and show that cGAS activation by genotoxic stress is rare and uncoupled from micronuclei. The study implicates R-loop structures and subtypes of chromatin bridges as potential cGAS activators.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"28 9","pages":"1957-1971"},"PeriodicalIF":22.7,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41556-026-02037-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148769323","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

Mechanisms underlying propagation of ferroptotic cell death 铁致细胞死亡的增殖机制。

IF 22.7 1区生物学

Nature Cell Biology Pub Date : 2026-08-21 DOI: 10.1038/s41556-026-02053-0

Francesca Maremonti, Alireza Dehdari, Nadja Leinung, Derek A. Pratt, Andreas Linkermann

{"title":"Mechanisms underlying propagation of ferroptotic cell death","authors":"Francesca Maremonti, Alireza Dehdari, Nadja Leinung, Derek A. Pratt, Andreas Linkermann","doi":"10.1038/s41556-026-02053-0","DOIUrl":"10.1038/s41556-026-02053-0","url":null,"abstract":"Necrotic zones in tissues occur in a wide variety of diseases. Ferroptosis, an iron-promoted necrosis driven by lipid peroxidation, has been identified as a key cell death modality in these conditions. Cells undergoing ferroptosis are unique in that they can induce death in their neighbours. Here we review salient aspects of ferroptosis propagation on the molecular, cellular and tissue levels. Cell death propagation is restricted by several ferroptosis-suppression systems. Glutathione peroxidase 4 (GPX4) and ferroptosis-suppressor protein 1 (FSP1) are now well established as master regulators, but various additional systems dictate ferroptosis sensitivity. We discuss how these mechanisms contribute to the suppression of cell death propagation, and how they cause various tissues to be more or less resistant to ferroptosis propagation. Understanding tissue-specific dynamics is critical to interpret the beneficial effects and limitations of future therapeutic approaches for ferroptosis-driven diseases. This Perspective discusses emerging evidence for non-cell-autonomous propagation of ferroptotic cell death and highlights the mechanisms that underlie its restriction in tissues, as well as ferroptosis surveillance beyond the cellular level.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"28 9","pages":"1788-1798"},"PeriodicalIF":22.7,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795861","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 lipid kinase joins the transcriptional machinery 脂质激酶加入了转录机制。

IF 22.7 1区生物学

Nature Cell Biology Pub Date : 2026-08-20 DOI: 10.1038/s41556-026-02046-z

Fernanda Rezende Pabst, Daphne Selvaggia Cabianca

引用次数: 0

Evading disulfidptosis via NRF2 translation 通过NRF2翻译避免二翘。

IF 22.7 1区生物学

Nature Cell Biology Pub Date : 2026-08-14 DOI: 10.1038/s41556-026-02036-1

Liam Baird, Masayuki Yamamoto

引用次数: 0