PLoS Biology最新文献_第10页

Microglia cannibalism and efferocytosis leads to shorter lifespans of developmental microglia. 小胶质细胞食人和排泄导致发育期小胶质细胞寿命缩短

IF 9.8 1区生物学

PLoS Biology Pub Date : 2024-10-30 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002819

Hannah Gordon, Zachary T Schafer, Cody J Smith

{"title":"Microglia cannibalism and efferocytosis leads to shorter lifespans of developmental microglia.","authors":"Hannah Gordon, Zachary T Schafer, Cody J Smith","doi":"10.1371/journal.pbio.3002819","DOIUrl":"10.1371/journal.pbio.3002819","url":null,"abstract":"The overproduction of cells and subsequent production of debris is a universal principle of neurodevelopment. Here, we show an additional feature of the developing nervous system that causes neural debris-promoted by the sacrificial nature of embryonic microglia that irreversibly become phagocytic after clearing other neural debris. Described as long-lived, microglia colonize the embryonic brain and persist into adulthood. Using transgenic zebrafish to investigate the microglia debris during brain construction, we identified that unlike other neural cell types that die in developmental stages after they have expanded, necroptosis-dependent microglial debris is prevalent when microglia are expanding in the zebrafish brain. Time-lapse imaging of microglia demonstrates that this debris is cannibalized by other microglia. To investigate features that promote microglia death and cannibalism, we used time-lapse imaging and fate-mapping strategies to track the lifespan of individual developmental microglia. These approaches revealed that instead of embryonic microglia being long-lived cells that completely digest their phagocytic debris, once most developmental microglia in zebrafish become phagocytic they eventually die, including ones that are cannibalistic. These results establish a paradox-which we tested by increasing neural debris and manipulating phagocytosis-that once most microglia in the embryo become phagocytic, they die, create debris, and then are cannibalized by other microglia, resulting in more phagocytic microglia that are destined to die.","PeriodicalId":49001,"journal":{"name":"PLoS Biology","volume":"22 10","pages":"e3002819"},"PeriodicalIF":9.8,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11524473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142548519","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 promises and challenges of neurotechnology to improve human health and cognition. 神经技术在改善人类健康和认知方面的前景与挑战。

IF 9.8 1区生物学

PLoS Biology Pub Date : 2024-10-30 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002903

Simon Hanslmayr

引用次数: 0

Can neurotechnology revolutionize cognitive enhancement? 神经技术能否彻底改变认知能力的提高？

IF 9.8 1区生物学

PLoS Biology Pub Date : 2024-10-29 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002831

Ines R Violante, Prince Okyere

引用次数: 0

Closing the sensory feedback loop is necessary for effective neurorehabilitation. 关闭感觉反馈回路是有效神经康复的必要条件。

IF 9.8 1区生物学

PLoS Biology Pub Date : 2024-10-29 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002866

Andrea Cimolato, Stanisa Raspopovic

引用次数: 0

The future of transcranial ultrasound as a precision brain interface. 经颅超声作为精确脑接口的未来。

IF 9.8 1区生物学

PLoS Biology Pub Date : 2024-10-29 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002884

Keith Murphy, Elsa Fouragnan

{"title":"The future of transcranial ultrasound as a precision brain interface.","authors":"Keith Murphy, Elsa Fouragnan","doi":"10.1371/journal.pbio.3002884","DOIUrl":"https://doi.org/10.1371/journal.pbio.3002884","url":null,"abstract":"Our understanding of brain circuit operations and disorders has rapidly outpaced our ability to intervene and restore them. Developing technologies that can precisely interface with any brain region and circuit may combine diagnostics with therapeutic intervention, expediting personalised brain medicine. Transcranial ultrasound stimulation (TUS) is a promising noninvasive solution to this challenge, offering focal precision and scalability. By exploiting the biomechanics of pressure waves on brain tissue, TUS enables multi-site targeted neuromodulation across distributed circuits in the cortex and deeper areas alike. In this Essay, we explore the emergent evidence that TUS can functionally test and modify dysfunctional regions, effectively serving as a search and rescue tool for the brain. We define the challenges and opportunities faced by TUS as it moves towards greater target precision and integration with advanced brain monitoring and interventional technology. Finally, we propose a roadmap for the evolution of TUS as it progresses from a research tool to a clinically validated therapeutic for brain disorders.","PeriodicalId":49001,"journal":{"name":"PLoS Biology","volume":"22 10","pages":"e3002884"},"PeriodicalIF":9.8,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11521279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142548520","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

MICU2 up-regulation enhances tumor aggressiveness and metabolic reprogramming during colorectal cancer development. MICU2 的上调增强了结直肠癌发展过程中的肿瘤侵袭性和代谢重编程。

IF 9.8 1区生物学

PLoS Biology Pub Date : 2024-10-28 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002854

Alison Robert, David Crottès, Jérôme Bourgeais, Naig Gueguen, Arnaud Chevrollier, Jean-François Dumas, Stéphane Servais, Isabelle Domingo, Stéphanie Chadet, Julien Sobilo, Olivier Hérault, Thierry Lecomte, Christophe Vandier, William Raoul, Maxime Guéguinou

{"title":"MICU2 up-regulation enhances tumor aggressiveness and metabolic reprogramming during colorectal cancer development.","authors":"Alison Robert, David Crottès, Jérôme Bourgeais, Naig Gueguen, Arnaud Chevrollier, Jean-François Dumas, Stéphane Servais, Isabelle Domingo, Stéphanie Chadet, Julien Sobilo, Olivier Hérault, Thierry Lecomte, Christophe Vandier, William Raoul, Maxime Guéguinou","doi":"10.1371/journal.pbio.3002854","DOIUrl":"10.1371/journal.pbio.3002854","url":null,"abstract":"The mitochondrial Ca2+ uniporter (MCU) plays crucial role in intramitochondrial Ca2+ uptake, allowing Ca2+-dependent activation of oxidative metabolism. In recent decades, the role of MCU pore-forming proteins has been highlighted in cancer. However, the contribution of MCU-associated regulatory proteins mitochondrial calcium uptake 1 and 2 (MICU1 and MICU2) to pathophysiological conditions has been poorly investigated. Here, we describe the role of MICU2 in cell proliferation and invasion using in vitro and in vivo models of human colorectal cancer (CRC). Transcriptomic analysis demonstrated an increase in MICU2 expression and the MICU2/MICU1 ratio in advanced CRC and CRC-derived metastases. We report that expression of MICU2 is necessary for mitochondrial Ca2+ uptake and quality of the mitochondrial network. Our data reveal the interplay between MICU2 and MICU1 in the metabolic flexibility between anaerobic glycolysis and OXPHOS. Overall, our study sheds light on the potential role of the MICUs in diseases associated with metabolic reprogramming.","PeriodicalId":49001,"journal":{"name":"PLoS Biology","volume":"22 10","pages":"e3002854"},"PeriodicalIF":9.8,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11542858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142523370","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

Ethical considerations for the use of brain-computer interfaces for cognitive enhancement. 使用脑机接口增强认知能力的伦理考虑。

IF 9.8 1区生物学

PLoS Biology Pub Date : 2024-10-28 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002899

Emma C Gordon, Anil K Seth

引用次数: 0

The expanding horizon of neurotechnology: Is multimodal neuromodulation the future? 神经技术的视野不断扩大：多模态神经调控是未来的趋势吗？

IF 9.8 1区生物学

PLoS Biology Pub Date : 2024-10-28 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002885

Silvestro Micera, Guglielmo Foffani

引用次数: 0

The future of quantum technologies for brain imaging. 脑成像量子技术的未来。

IF 9.8 1区生物学

PLoS Biology Pub Date : 2024-10-28 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002824

Daniele Faccio

引用次数: 0

Structure of G protein-coupled receptor GPR1 bound to full-length chemerin adipokine reveals a chemokine-like reverse binding mode. 与全长螯合素脂肪因子结合的 G 蛋白偶联受体 GPR1 的结构揭示了一种类似于趋化因子的反向结合模式。

IF 9.8 1区生物学

PLoS Biology Pub Date : 2024-10-28 eCollection Date: 2024-10-01 DOI: 10.1371/journal.pbio.3002838

Aijun Liu, Yezhou Liu, Geng Chen, Wenping Lyu, Fang Ye, Junlin Wang, Qiwen Liao, Lizhe Zhu, Yang Du, Richard D Ye

{"title":"Structure of G protein-coupled receptor GPR1 bound to full-length chemerin adipokine reveals a chemokine-like reverse binding mode.","authors":"Aijun Liu, Yezhou Liu, Geng Chen, Wenping Lyu, Fang Ye, Junlin Wang, Qiwen Liao, Lizhe Zhu, Yang Du, Richard D Ye","doi":"10.1371/journal.pbio.3002838","DOIUrl":"10.1371/journal.pbio.3002838","url":null,"abstract":"Chemerin is an adipokine with chemotactic activity to a subset of leukocytes. Chemerin binds to 3 G protein-coupled receptors, including chemokine-like receptor 1 (CMKLR1), G protein-coupled receptor 1 (GPR1), and C-C chemokine receptor-like 2 (CCRL2). Here, we report that GPR1 is capable of Gi signaling when stimulated with full-length chemerin or its C-terminal nonapeptide (C9, YFPGQFAFS). We present high-resolution cryo-EM structures of Gi-coupled GPR1 bound to full-length chemerin and to the C9 peptide, respectively. C9 insertion into the transmembrane (TM) binding pocket is both necessary and sufficient for GPR1 signaling, whereas the full-length chemerin uses its bulky N-terminal core for interaction with a β-strand located at the N-terminus of GPR1. This interaction involves multiple β-strands of full-length chemerin, forming a β-sheet that serves as a \"lid\" for the TM binding pocket and is energetically expensive to remove as indicated by molecular dynamics simulations with free energy landscape analysis. Combining results from functional assays, our structural model explains why C9 is an activating peptide at GPR1 and how the full-length chemerin uses a \"two-site\" model for enhanced interaction with GPR1.","PeriodicalId":49001,"journal":{"name":"PLoS Biology","volume":"22 10","pages":"e3002838"},"PeriodicalIF":9.8,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11515964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142523373","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