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Peroxisomes are underappreciated organelles hijacked by viruses. 过氧物酶体是被病毒劫持的细胞器，但人们对它的认识不足。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2024-12-11 DOI: 10.1016/j.tcb.2024.11.006
Marie Villares, Lucile Espert, Coralie F Daussy
{"title":"Peroxisomes are underappreciated organelles hijacked by viruses.","authors":"Marie Villares, Lucile Espert, Coralie F Daussy","doi":"10.1016/j.tcb.2024.11.006","DOIUrl":"https://doi.org/10.1016/j.tcb.2024.11.006","url":null,"abstract":"<p><p>Peroxisomes are cellular organelles that are crucial for metabolism, stress responses, and healthy aging. They have recently come to be considered as important mediators of the immune response during viral infections. Consequently, various viruses target peroxisomes for the purpose of hijacking either their biogenesis or their functions, as a means of replicating efficiently, making this a compelling research area. Despite their known connections with mitochondria, which have been the object of considerable research on account of their role in the innate immune response, less is known about peroxisomes in this context. In this review, we explore the evolving understanding of the role of peroxisomes, highlighting recent findings on how they are exploited by viruses to modulate their replication cycle.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142819961","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
Death by ribosome. 核糖体致死。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2024-12-10 DOI: 10.1016/j.tcb.2024.10.013
Anna Constance Vind, Franklin L Zhong, Simon Bekker-Jensen
{"title":"Death by ribosome.","authors":"Anna Constance Vind, Franklin L Zhong, Simon Bekker-Jensen","doi":"10.1016/j.tcb.2024.10.013","DOIUrl":"https://doi.org/10.1016/j.tcb.2024.10.013","url":null,"abstract":"<p><p>Next to their essential role as protein production factories, ribosomes serve as molecular sensors of cell stress. Stalled and collided ribosomes trigger specific stress signaling, including the ribotoxic stress response (RSR). The RSR is initiated by the mitogen-activated protein (MAP)-3 kinase ZAKα in response to a plethora of translational aberrations, leading to activation of the stress-activated MAP kinases p38 and jun N-terminal kinase (JNK). Recent insights have highlighted an important role for the RSR pathway in triggering programmed cell death processes, including apoptosis and pyroptosis, in a broad range of physiologically relevant conditions. In this review, we summarize recent work on known links between programmed and accidental ribosome toxicity, RSR signaling, and cell death.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142815096","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
Proteome-wide CETSA reveals new step in apoptosis control. 全蛋白质组 CETSA 揭示了细胞凋亡控制的新步骤。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2024-12-01 Epub Date: 2024-11-19 DOI: 10.1016/j.tcb.2024.11.001
Inna N Lavrik, Nikita V Ivanisenko
{"title":"Proteome-wide CETSA reveals new step in apoptosis control.","authors":"Inna N Lavrik, Nikita V Ivanisenko","doi":"10.1016/j.tcb.2024.11.001","DOIUrl":"10.1016/j.tcb.2024.11.001","url":null,"abstract":"<p><p>Apoptosis, a well-established program of cell death, is fundamental to all multicellular organisms. Recent studies of apoptosis initiation events using proteome-wide cellular thermal shift assay (CETSA) have revealed a novel regulatory mechanism involving the cleavage of nuclear substrates. This finding suggests a previously unrecognized amplification step in apoptosis occurring within the nucleus.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":"986-987"},"PeriodicalIF":13.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142683774","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
Cutting through the stress: RNA decay pathways at the endoplasmic reticulum. 切断应激:内质网的RNA衰变途径。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2024-12-01 Epub Date: 2023-11-25 DOI: 10.1016/j.tcb.2023.11.003
Franziska Ottens, Sotirios Efstathiou, Thorsten Hoppe
{"title":"Cutting through the stress: RNA decay pathways at the endoplasmic reticulum.","authors":"Franziska Ottens, Sotirios Efstathiou, Thorsten Hoppe","doi":"10.1016/j.tcb.2023.11.003","DOIUrl":"10.1016/j.tcb.2023.11.003","url":null,"abstract":"<p><p>The endoplasmic reticulum (ER) is central to the processing of luminal, transmembrane, and secretory proteins, and maintaining a functional ER is essential for organismal physiology and health. Increased protein-folding load on the ER causes ER stress, which activates quality control mechanisms to restore ER function and protein homeostasis. Beyond protein quality control, mRNA decay pathways have emerged as potent ER fidelity regulators, but their mechanistic roles in ER quality control and their interrelationships remain incompletely understood. Herein, we review ER-associated RNA decay pathways - including regulated inositol-requiring enzyme 1α (IRE1α)-dependent mRNA decay (RIDD), nonsense-mediated mRNA decay (NMD), and Argonaute-dependent RNA silencing - in ER homeostasis, and highlight the intricate coordination of ER-targeted RNA and protein decay mechanisms and their association with antiviral defense.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":"1056-1068"},"PeriodicalIF":13.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138441786","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
(Alternative) transcription start sites as regulators of RNA processing. (替代）转录起始位点是 RNA 加工的调节器。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2024-12-01 Epub Date: 2024-03-25 DOI: 10.1016/j.tcb.2024.02.010
Carlos Alfonso-Gonzalez, Valérie Hilgers
{"title":"(Alternative) transcription start sites as regulators of RNA processing.","authors":"Carlos Alfonso-Gonzalez, Valérie Hilgers","doi":"10.1016/j.tcb.2024.02.010","DOIUrl":"10.1016/j.tcb.2024.02.010","url":null,"abstract":"<p><p>Alternative transcription start site usage (ATSS) is a widespread regulatory strategy that enables genes to choose between multiple genomic loci for initiating transcription. This mechanism is tightly controlled during development and is often altered in disease states. In this review, we examine the growing evidence highlighting a role for transcription start sites (TSSs) in the regulation of mRNA isoform selection during and after transcription. We discuss how the choice of transcription initiation sites influences RNA processing and the importance of this crosstalk for cell identity and organism function. We also speculate on possible mechanisms underlying the integration of transcriptional and post-transcriptional processes.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":"1018-1028"},"PeriodicalIF":13.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140295376","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
Increased O-GlcNAcylation connects metabolic to transcriptional reprogramming during pathophysiological cell activation. 在病理生理细胞激活过程中，O-GlcNAcylation 的增加将代谢与转录重编程联系起来。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2024-12-01 Epub Date: 2024-11-07 DOI: 10.1016/j.tcb.2024.10.007
Ninon Very, Bart Staels, Jérôme Eeckhoute
{"title":"Increased O-GlcNAcylation connects metabolic to transcriptional reprogramming during pathophysiological cell activation.","authors":"Ninon Very, Bart Staels, Jérôme Eeckhoute","doi":"10.1016/j.tcb.2024.10.007","DOIUrl":"10.1016/j.tcb.2024.10.007","url":null,"abstract":"<p><p>Increased protein O-linked β-N-acetylglucosaminylation (O-GlcNAcylation) has emerged as a hallmark of mammalian cell activation, contributing to Warburg-like metabolic rewiring allowing the acquisition of new functionalities. Recent advances indicate that O-GlcNAcylation promotes the activity of transcriptional regulators driving gene expression reprogramming. This may offer new therapeutic opportunities in a broad spectrum of pathological conditions.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":"988-991"},"PeriodicalIF":13.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142633154","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
Unlocking mechanosensitivity: integrins in neural adaptation. 解开机械敏感性：神经适应中的整合素
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2024-12-01 Epub Date: 2024-03-20 DOI: 10.1016/j.tcb.2024.02.011
Fanny Jaudon, Lorenzo A Cingolani
{"title":"Unlocking mechanosensitivity: integrins in neural adaptation.","authors":"Fanny Jaudon, Lorenzo A Cingolani","doi":"10.1016/j.tcb.2024.02.011","DOIUrl":"10.1016/j.tcb.2024.02.011","url":null,"abstract":"<p><p>Mechanosensitivity extends beyond sensory cells to encompass most neurons in the brain. Here, we explore recent research on the role of integrins, a diverse family of adhesion molecules, as crucial biomechanical sensors translating mechanical forces into biochemical and electrical signals in the brain. The varied biomechanical properties of neuronal integrins, including their force-dependent conformational states and ligand interactions, dictate their specific functions. We discuss new findings on how integrins regulate filopodia and dendritic spines, shedding light on their contributions to synaptic plasticity, and explore recent discoveries on how they engage with metabotropic receptors and ion channels, highlighting their direct participation in electromechanical transduction. Finally, to facilitate a deeper understanding of these developments, we present molecular and biophysical models of mechanotransduction.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":"1029-1043"},"PeriodicalIF":13.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140186403","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
Epigenetic control of circadian clocks by environmental signals. 环境信号对昼夜节律钟的表观遗传控制
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2024-12-01 Epub Date: 2024-02-28 DOI: 10.1016/j.tcb.2024.02.005
Xiao-Lan Liu, Zeyu Duan, Muqun Yu, Xiao Liu
{"title":"Epigenetic control of circadian clocks by environmental signals.","authors":"Xiao-Lan Liu, Zeyu Duan, Muqun Yu, Xiao Liu","doi":"10.1016/j.tcb.2024.02.005","DOIUrl":"10.1016/j.tcb.2024.02.005","url":null,"abstract":"<p><p>Circadian clocks have evolved to enable organisms to respond to daily environmental changes. Maintaining a robust circadian rhythm under various perturbations and stresses is essential for the fitness of an organism. In the core circadian oscillator conserved in eukaryotes (from fungi to mammals), a negative feedback loop based on both transcription and translation drives circadian rhythms. The expression of circadian clock genes depends both on the binding of transcription activators at the promoter and on the chromatin state of the clock genes, and epigenetic modifications of chromatin are crucial for transcriptional regulation of circadian clock genes. Herein we review current knowledge of epigenetic regulation of circadian clock mechanisms and discuss how environmental cues can control clock gene expression by affecting chromatin states.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":"992-1006"},"PeriodicalIF":13.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139998431","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
TFEB links the cGAS-STING pathway to lysosome biogenesis. TFEB 将 cGAS-STING 通路与溶酶体生物生成联系起来。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2024-12-01 Epub Date: 2024-11-14 DOI: 10.1016/j.tcb.2024.10.011
Yaping Meng, Xinran Li, Haoxing Xu
{"title":"TFEB links the cGAS-STING pathway to lysosome biogenesis.","authors":"Yaping Meng, Xinran Li, Haoxing Xu","doi":"10.1016/j.tcb.2024.10.011","DOIUrl":"10.1016/j.tcb.2024.10.011","url":null,"abstract":"<p><p>The cGAS-STING pathway senses the level of double-stranded (ds)DNA in the cytosol, and is required for innate immunity through its effector, TBK1. A recent study by Lv et al. reports that STING activation also simultaneously promotes lysosomal biogenesis by inducing nuclear translocation of the transcription factors TFEB/TFE3 independent of TBK1.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":"983-985"},"PeriodicalIF":13.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142640338","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
Transcription-coupled repair of DNA-protein crosslinks. dna -蛋白交联的转录偶联修复。
IF 13 1区 生物学
Trends in Cell Biology Pub Date : 2024-11-30 DOI: 10.1016/j.tcb.2024.11.003
Christopher J Carnie, Stephen P Jackson, Julian Stingele
{"title":"Transcription-coupled repair of DNA-protein crosslinks.","authors":"Christopher J Carnie, Stephen P Jackson, Julian Stingele","doi":"10.1016/j.tcb.2024.11.003","DOIUrl":"https://doi.org/10.1016/j.tcb.2024.11.003","url":null,"abstract":"<p><p>DNA-protein crosslinks (DPCs) are highly toxic DNA lesions that are relevant to multiple human diseases. They are caused by various endogenous and environmental agents, and from the actions of enzymes such as topoisomerases. DPCs impede DNA polymerases, triggering replication-coupled DPC repair. Until recently the consequences of DPC blockade of RNA polymerases remained unclear. New methodologies for studying DPC repair have enabled the discovery of a transcription-coupled (TC) DPC repair pathway. Briefly, RNA polymerase II (RNAPII) stalling initiates TC-DPC repair, leading to sequential engagement of Cockayne syndrome (CS) proteins CSB and CSA, and to proteasomal degradation of the DPC. Deficient TC-DPC repair caused by loss of CSA or CSB function may help to explain the complex clinical presentation of CS patients.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142774760","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
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