{"title":"Stewarding AI in agriculture research","authors":"Ismahane Elouafi","doi":"10.1126/science.aef0964","DOIUrl":"10.1126/science.aef0964","url":null,"abstract":"","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Qiang Zhang, Huamin Li, Peiping Yu, Pengyu Liu, Ning Sun, Yiyan Wang, Chunlai Tu, Yiping Liu, Yan Wang, Xinyang Yue, Linlin Ma, Wen Wen, Jinyang Xu, Zhaofeng Liang, Jingyuan Ma, Fei Song, Zheng Liang, Hao Sun, Daishun Ling, Hongyan Liang, Feng Liu, Yongfeng Hu, Tao Cheng, Jun Li
Electrochemical lithium (Li)–mediated nitrogen (N2) reduction could enable production of ammonia (NH3) at ambient temperatures and pressures, offering a route to reduce carbon emissions in the chemical sector. However, NH3 productivity is often limited by sluggish Li-ion desolvation and diffusion at the solid electrolyte interphase (SEI). Here, we present a concerted desolvation:diffusion layered SEI architecture that provides abundant Li-ion flux for efficient N2 conversion toward NH3 production at high current densities. The SEI comprises stacked inorganic layers with low ion-binding affinity and high ion-conductivity functionalities that increase Li-ion flux by two orders of magnitude. This design strategy achieved N2 electroreduction in a 2 M lithium difluoro(oxalato)borate electrolyte with a Faradaic efficiency of 98% and an energy efficiency of 21% for NH3 production at 100 milliamperes per square centimeter (mA cm−2). The system sustained an 80% Faradaic efficiency over 40 hours, after which performance declined.
电化学锂（Li）介导的氮（N2）还原可以在环境温度和压力下生产氨（NH3），为减少化学行业的碳排放提供了一条途径。然而，NH3的生产效率往往受到锂离子在固体电解质界面（SEI）缓慢的溶解和扩散的限制。在这里，我们提出了一种协调的脱溶：扩散层状SEI结构，它提供了丰富的锂离子通量，在高电流密度下有效地将N2转化为NH3。SEI包括堆叠的无机层，具有低离子结合亲和力和高离子电导率功能，可将锂离子通量提高两个数量级。该设计策略在2 M二氟锂（草酸）硼酸盐电解质中实现了N2电还原，法拉第效率为98%，在100毫安/平方厘米（mA cm - 2）下产生NH3的能量效率为21%。该系统在40小时内保持了80%的法拉第效率，之后性能下降。
{"title":"Enhanced Li-ion diffusion improves N2-to-NH3 current efficiency at 100 mA cm−2","authors":"Qiang Zhang, Huamin Li, Peiping Yu, Pengyu Liu, Ning Sun, Yiyan Wang, Chunlai Tu, Yiping Liu, Yan Wang, Xinyang Yue, Linlin Ma, Wen Wen, Jinyang Xu, Zhaofeng Liang, Jingyuan Ma, Fei Song, Zheng Liang, Hao Sun, Daishun Ling, Hongyan Liang, Feng Liu, Yongfeng Hu, Tao Cheng, Jun Li","doi":"10.1126/science.adw5462","DOIUrl":"10.1126/science.adw5462","url":null,"abstract":"<div >Electrochemical lithium (Li)–mediated nitrogen (N<sub>2</sub>) reduction could enable production of ammonia (NH<sub>3</sub>) at ambient temperatures and pressures, offering a route to reduce carbon emissions in the chemical sector. However, NH<sub>3</sub> productivity is often limited by sluggish Li-ion desolvation and diffusion at the solid electrolyte interphase (SEI). Here, we present a concerted desolvation:diffusion layered SEI architecture that provides abundant Li-ion flux for efficient N<sub>2</sub> conversion toward NH<sub>3</sub> production at high current densities. The SEI comprises stacked inorganic layers with low ion-binding affinity and high ion-conductivity functionalities that increase Li-ion flux by two orders of magnitude. This design strategy achieved N<sub>2</sub> electroreduction in a 2 M lithium difluoro(oxalato)borate electrolyte with a Faradaic efficiency of 98% and an energy efficiency of 21% for NH<sub>3</sub> production at 100 milliamperes per square centimeter (mA cm<sup>−2</sup>). The system sustained an 80% Faradaic efficiency over 40 hours, after which performance declined.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marc S. Lavine, Jesse Smith, Keith T. Smith, Phil Szuromi, Madeleine Seale, Sacha Vignieri, Melissa L. Norton, John Foley, Bianca Lopez, Mattia Maroso, Di Jiang, Yevgeniya Nusinovich, Sarah H. Ross, Michael A. Funk, Jake S. Yeston, Leoma Bere
{"title":"In Science Journals","authors":"Marc S. Lavine, Jesse Smith, Keith T. Smith, Phil Szuromi, Madeleine Seale, Sacha Vignieri, Melissa L. Norton, John Foley, Bianca Lopez, Mattia Maroso, Di Jiang, Yevgeniya Nusinovich, Sarah H. Ross, Michael A. Funk, Jake S. Yeston, Leoma Bere","doi":"10.1126/science.aeg3196","DOIUrl":"10.1126/science.aeg3196","url":null,"abstract":"","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kishalay De, Morgan MacLeod, Jacob E. Jencson, Elizabeth Lovegrove, Andrea Antoni, Erin Kara, Mansi M. Kasliwal, Ryan M. Lau, Abraham Loeb, Megan Masterson, Aaron M. Meisner, Christos Panagiotou, Eliot Quataert, Robert Simcoe
When a massive star reaches the end of its lifetime, its core collapses and releases neutrinos that drive a shock into the outer layers (the stellar envelope). A sufficiently strong shock ejects the envelope, producing a supernova. If the shock fails to eject it, the envelope is predicted to fall back onto the collapsing core, producing a stellar-mass black hole (BH) and causing the star to disappear. We report observations of M31-2014-DS1, a hydrogen-depleted supergiant in the Andromeda Galaxy. In 2014, it brightened in the mid-infrared, then from 2017 to 2022, it faded by factors of in optical light (becoming undetectable) and in total light. We interpret these observations, and those of a previous event in NGC 6946, as evidence for failed supernovae forming stellar-mass BHs.
{"title":"Disappearance of a massive star in the Andromeda Galaxy due to formation of a black hole","authors":"Kishalay De, Morgan MacLeod, Jacob E. Jencson, Elizabeth Lovegrove, Andrea Antoni, Erin Kara, Mansi M. Kasliwal, Ryan M. Lau, Abraham Loeb, Megan Masterson, Aaron M. Meisner, Christos Panagiotou, Eliot Quataert, Robert Simcoe","doi":"10.1126/science.adt4853","DOIUrl":"10.1126/science.adt4853","url":null,"abstract":"<div >When a massive star reaches the end of its lifetime, its core collapses and releases neutrinos that drive a shock into the outer layers (the stellar envelope). A sufficiently strong shock ejects the envelope, producing a supernova. If the shock fails to eject it, the envelope is predicted to fall back onto the collapsing core, producing a stellar-mass black hole (BH) and causing the star to disappear. We report observations of M31-2014-DS1, a hydrogen-depleted supergiant in the Andromeda Galaxy. In 2014, it brightened in the mid-infrared, then from 2017 to 2022, it faded by factors of <span><math><mrow><mo>≳</mo><msup><mrow><mn>10</mn></mrow><mn>4</mn></msup></mrow></math></span> in optical light (becoming undetectable) and <span><math><mrow><mo>≳</mo><mn>10</mn></mrow></math></span> in total light. We interpret these observations, and those of a previous event in NGC 6946, as evidence for failed supernovae forming stellar-mass BHs.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Josephine Elena Reek, Constantin M. Zohner, Gabriel Reuben Smith, Susan C. Cook-Patton, Pieter De Frenne, Paolo D’Odorico, Marius G. Floriancic, Robert B. Jackson, Julia A. Jones, James W. Kirchner, Marysa Laguë, Yuting Liang, Yuta J. Masuda, Robert I. McDonald, Luke A. Parsons, Benedict S. Probst, June T. Spector, Thales A. P. West, Nicholas H. Wolff, Florian Zellweger, Thomas W. Crowther
Forests regulate global and local climates in ways that impact human well-being. In this Review, we discuss the scale-dependent mechanisms through which forests regulate climate, highlighting their contributions to global mitigation and local adaptation. Locally, forests tend to buffer temperatures, cooling in warm conditions and warming in cold ones. In regions that naturally support dense forest cover, trees contribute to global cooling primarily through carbon uptake, with some offsetting from albedo-related warming. By enhancing rainfall interception, evapotranspiration, and cloud formation, forests also influence the hydrological cycle, lowering flood risks in humid regions but often reducing downstream water availability, especially in drier climates. Collectively, these interacting processes show that the greatest climate benefits occur where forests are native, highlighting their importance for both climate adaptation and mitigation.
{"title":"More than mitigation: The role of forests in climate adaptation","authors":"Josephine Elena Reek, Constantin M. Zohner, Gabriel Reuben Smith, Susan C. Cook-Patton, Pieter De Frenne, Paolo D’Odorico, Marius G. Floriancic, Robert B. Jackson, Julia A. Jones, James W. Kirchner, Marysa Laguë, Yuting Liang, Yuta J. Masuda, Robert I. McDonald, Luke A. Parsons, Benedict S. Probst, June T. Spector, Thales A. P. West, Nicholas H. Wolff, Florian Zellweger, Thomas W. Crowther","doi":"10.1126/science.ads4361","DOIUrl":"10.1126/science.ads4361","url":null,"abstract":"<div >Forests regulate global and local climates in ways that impact human well-being. In this Review, we discuss the scale-dependent mechanisms through which forests regulate climate, highlighting their contributions to global mitigation and local adaptation. Locally, forests tend to buffer temperatures, cooling in warm conditions and warming in cold ones. In regions that naturally support dense forest cover, trees contribute to global cooling primarily through carbon uptake, with some offsetting from albedo-related warming. By enhancing rainfall interception, evapotranspiration, and cloud formation, forests also influence the hydrological cycle, lowering flood risks in humid regions but often reducing downstream water availability, especially in drier climates. Collectively, these interacting processes show that the greatest climate benefits occur where forests are native, highlighting their importance for both climate adaptation and mitigation.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jared W. Westbrook, Joanna Malukiewicz, Qian Zhang, Avinash Sreedasyam, Jerry W. Jenkins, Vasiliy Lakoba, Sara Fitzsimmons, Jamie Van Clief, Kendra Collins, Stephen Hoy, Cassie Stark, Lake Graboski, Eric Jenkins, Thomas M. Saielli, Benjamin T. Jarrett, Lucinda J. Wigfield, Lauren M. Kerwien, Ciera Wilbur, Alexander M. Sandercock, J. Hill Craddock, Susanna Keriö, Tetyana Zhebentyayeva, Shenghua Fan, Austin M. Thomas, Albert G. Abbott, C. Dana Nelson, Xiaoxia Xia, James R. McKenna, Caleb Kell, Melissa Williams, LoriBeth Boston, Christopher Plott, Florian Carle, Jack Swatt, Jack Ostroff, Steven N. Jeffers, Kathleen McKeever, Erica Smith, Thomas J. Ellis, Joseph B. James, Paul Sisco, Andrew Newhouse, Erik Carlson, William A. Powell, Frederick V. Hebard, John Scrivani, Caragh Heverly, Martin Cipollini, Brian Clark, Eric Evans, Bruce Levine, John E. Carlson, David Goodstein, Jack Orebaugh, Zamin K. Yang, Madhavi Z. Martin, Joanna Tannous, Tomás A. Rush, Nancy L. Engle, Timothy J. Tschaplinski, Jane Grimwood, Jeremy Schmutz, Jason A. Holliday, John T. Lovell
More than a century after two introduced pathogens killed billions of American chestnut trees, introgression of resistance alleles from Chinese chestnuts has contributed to the recovery of self-sustaining populations. However, progress has been slow because of the complex genetic architecture of resistance. To better understand blight resistance, we compared reference genomes, gene expression responses, and stem metabolite profiles of the resistant Chinese and susceptible American chestnut species. To accelerate resistance breeding, we conducted large-scale phenotyping and genotyping in hybrids of these species. Simulation and inoculation experiments suggest that significant resistance gains are possible through selectively breeding trees with an average of 70 to 85% American chestnut ancestry. The resources developed in this work are foundational for breeding to create diverse restoration populations with sufficient disease resistance and competitive growth.
{"title":"Genomic approaches to accelerate American chestnut restoration","authors":"Jared W. Westbrook, Joanna Malukiewicz, Qian Zhang, Avinash Sreedasyam, Jerry W. Jenkins, Vasiliy Lakoba, Sara Fitzsimmons, Jamie Van Clief, Kendra Collins, Stephen Hoy, Cassie Stark, Lake Graboski, Eric Jenkins, Thomas M. Saielli, Benjamin T. Jarrett, Lucinda J. Wigfield, Lauren M. Kerwien, Ciera Wilbur, Alexander M. Sandercock, J. Hill Craddock, Susanna Keriö, Tetyana Zhebentyayeva, Shenghua Fan, Austin M. Thomas, Albert G. Abbott, C. Dana Nelson, Xiaoxia Xia, James R. McKenna, Caleb Kell, Melissa Williams, LoriBeth Boston, Christopher Plott, Florian Carle, Jack Swatt, Jack Ostroff, Steven N. Jeffers, Kathleen McKeever, Erica Smith, Thomas J. Ellis, Joseph B. James, Paul Sisco, Andrew Newhouse, Erik Carlson, William A. Powell, Frederick V. Hebard, John Scrivani, Caragh Heverly, Martin Cipollini, Brian Clark, Eric Evans, Bruce Levine, John E. Carlson, David Goodstein, Jack Orebaugh, Zamin K. Yang, Madhavi Z. Martin, Joanna Tannous, Tomás A. Rush, Nancy L. Engle, Timothy J. Tschaplinski, Jane Grimwood, Jeremy Schmutz, Jason A. Holliday, John T. Lovell","doi":"10.1126/science.adw3225","DOIUrl":"10.1126/science.adw3225","url":null,"abstract":"<div >More than a century after two introduced pathogens killed billions of American chestnut trees, introgression of resistance alleles from Chinese chestnuts has contributed to the recovery of self-sustaining populations. However, progress has been slow because of the complex genetic architecture of resistance. To better understand blight resistance, we compared reference genomes, gene expression responses, and stem metabolite profiles of the resistant Chinese and susceptible American chestnut species. To accelerate resistance breeding, we conducted large-scale phenotyping and genotyping in hybrids of these species. Simulation and inoculation experiments suggest that significant resistance gains are possible through selectively breeding trees with an average of 70 to 85% American chestnut ancestry. The resources developed in this work are foundational for breeding to create diverse restoration populations with sufficient disease resistance and competitive growth.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L-Carnitine (the form of carnitine found in animals) transports long-chain fatty acids into mitochondria, where they go through β-oxidation, producing energy (1). This process occurs primarily in organs that use fat as energy, such as cardiac and skeletal muscles. For humans who eat meat, most carnitine is obtained from food. However, ~25% of the supply of carnitine in omnivorous humans relies on de novo synthesis, which reaches >90% among strict vegetarians or vegans. Endogenous carnitine is synthesized in the liver and kidneys from two methylated amino acids, lysine and methionine (1). This requires the transfer of trimethyllysine from the cytosol to the mitochondrial matrix (the innermost part of the mitochondria), for conversion into hydroxytrimethyllysine (2). On page 688 of this issue, Auger et al. (3) report that a mitochondrial trimethyllysine transporter, SLC25A45, has a key role in fat consumption in mice.
{"title":"The bottleneck of fat burning","authors":"Angela M. Ramos-Lobo, Pierre Maechler","doi":"10.1126/science.aef2173","DOIUrl":"10.1126/science.aef2173","url":null,"abstract":"<div >L-Carnitine (the form of carnitine found in animals) transports long-chain fatty acids into mitochondria, where they go through β-oxidation, producing energy (<i>1</i>). This process occurs primarily in organs that use fat as energy, such as cardiac and skeletal muscles. For humans who eat meat, most carnitine is obtained from food. However, ~25% of the supply of carnitine in omnivorous humans relies on de novo synthesis, which reaches >90% among strict vegetarians or vegans. Endogenous carnitine is synthesized in the liver and kidneys from two methylated amino acids, lysine and methionine (<i>1</i>). This requires the transfer of trimethyllysine from the cytosol to the mitochondrial matrix (the innermost part of the mitochondria), for conversion into hydroxytrimethyllysine (<i>2</i>). On page 688 of this issue, Auger <i>et al.</i> (<i>3</i>) report that a mitochondrial trimethyllysine transporter, SLC25A45, has a key role in fat consumption in mice.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Organisms have developed a variety of mechanisms to cope with potentially harmful mutations. These mechanisms include gene duplication, redundancy of metabolic factors or pathways, and feedback loops, all of which create backup systems and hidden reserves that ensure cellular stability (1). On page 687 of this issue, El-Brolosy et al. (2) report on transcriptional adaptation, a dual feedback and feedforward mechanism that uses genetic redundancy to compensate for mutations in protein-coding genes. The authors report that cells transport decay fragments of mutant messenger RNAs (mRNAs) from the cytoplasm to the nucleus to up-regulate the transcription of so-called “adapting genes”—the mutated gene; its paralogs (genes that originated from the same duplication event); and, in some cases, biologically related genes. El-Brolosy et al. also leveraged their mechanistic understanding of transcriptional regulation to develop short nucleic acid sequences that can artificially activate target gene expression in cells.
{"title":"Keeping cells fit","authors":"Xavier Rambout, Lynne E. Maquat","doi":"10.1126/science.aee7910","DOIUrl":"10.1126/science.aee7910","url":null,"abstract":"<div >Organisms have developed a variety of mechanisms to cope with potentially harmful mutations. These mechanisms include gene duplication, redundancy of metabolic factors or pathways, and feedback loops, all of which create backup systems and hidden reserves that ensure cellular stability (<i>1</i>). On page 687 of this issue, El-Brolosy <i>et al</i>. (<i>2</i>) report on transcriptional adaptation, a dual feedback and feedforward mechanism that uses genetic redundancy to compensate for mutations in protein-coding genes. The authors report that cells transport decay fragments of mutant messenger RNAs (mRNAs) from the cytoplasm to the nucleus to up-regulate the transcription of so-called “adapting genes”—the mutated gene; its paralogs (genes that originated from the same duplication event); and, in some cases, biologically related genes. El-Brolosy <i>et al</i>. also leveraged their mechanistic understanding of transcriptional regulation to develop short nucleic acid sequences that can artificially activate target gene expression in cells.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"RNA comes close to copying itself","authors":"Robert F. Service","doi":"10.1126/science.aeg3559","DOIUrl":"10.1126/science.aeg3559","url":null,"abstract":"","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Donia Arafa, Julia van de Korput, Philipp N. Braaker, Kieran P. Higgins, Niels R. C. Meijns, Katy L. H. Marshall-Phelps, Julia Meng, Daniel Soong, Eleonora Scalia, Kyle Lathem, Marcus Keatinge, Claire Richmond, Anna Klingseisen, Marja Main, Sarah A. Neely, David W. Hampton, Greg J. Duncan, Geert J. Schenk, Marie Louise Groot, Siddharthan Chandran, Ben Emery, Antonio Luchicchi, Maarten H. P. Kole, Anna C. Williams, David A. Lyons
Myelin damage is a hallmark of several neurological disorders, but how it occurs remains to be fully understood. In this study, we found that early damage in zebrafish and rodent demyelination models is characterized by myelin swelling. We show, through live imaging, that myelin swelling does not always lead to myelin loss and that swellings can sometimes resolve, allowing sheaths to remodel. Increased neuronal activity during early demyelination exacerbates myelin damage, whereas reducing neuronal activity mitigates myelin swelling in both zebrafish and mice. In human multiple sclerosis tissue, myelin swelling is also dynamic and is prominent around active lesions. Our data indicate that myelin swelling is a conserved feature of demyelination and that damage to myelin sheaths can resolve, opening opportunities for targeting human disease.
{"title":"Myelin sheaths in the central nervous system can withstand damage and dynamically remodel","authors":"Donia Arafa, Julia van de Korput, Philipp N. Braaker, Kieran P. Higgins, Niels R. C. Meijns, Katy L. H. Marshall-Phelps, Julia Meng, Daniel Soong, Eleonora Scalia, Kyle Lathem, Marcus Keatinge, Claire Richmond, Anna Klingseisen, Marja Main, Sarah A. Neely, David W. Hampton, Greg J. Duncan, Geert J. Schenk, Marie Louise Groot, Siddharthan Chandran, Ben Emery, Antonio Luchicchi, Maarten H. P. Kole, Anna C. Williams, David A. Lyons","doi":"10.1126/science.adr4661","DOIUrl":"10.1126/science.adr4661","url":null,"abstract":"<div >Myelin damage is a hallmark of several neurological disorders, but how it occurs remains to be fully understood. In this study, we found that early damage in zebrafish and rodent demyelination models is characterized by myelin swelling. We show, through live imaging, that myelin swelling does not always lead to myelin loss and that swellings can sometimes resolve, allowing sheaths to remodel. Increased neuronal activity during early demyelination exacerbates myelin damage, whereas reducing neuronal activity mitigates myelin swelling in both zebrafish and mice. In human multiple sclerosis tissue, myelin swelling is also dynamic and is prominent around active lesions. Our data indicate that myelin swelling is a conserved feature of demyelination and that damage to myelin sheaths can resolve, opening opportunities for targeting human disease.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"391 6786","pages":""},"PeriodicalIF":45.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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