Pub Date : 2024-11-28DOI: 10.1038/s41564-024-01871-y
William Bakhache, Walker Symonds-Orr, Lauren McCormick, Patrick T. Dolan
Insertions and deletions (InDels) are essential to protein evolution. In RNA viruses, InDels contribute to the emergence of viruses with new phenotypes, including altered host engagement and tropism. However, the tolerance of viral proteins for InDels has not been extensively studied. Here, we conduct deep mutational scanning to map and quantify the mutational tolerance of a complete viral proteome to insertion, deletion and substitution. We engineered approximately 45,000 insertions, 6,000 deletions and 41,000 amino acid substitutions across the nearly 2,200 coding positions of the Enterovirus A71 proteome, quantifying their effects on viral fitness by population sequencing. The vast majority of InDels are lethal to the virus, tolerated at only a few hotspots. Some of these hotspots overlap with sites of host recognition and immune engagement, suggesting tolerance at these sites reflects the important role InDels have played in the past phenotypic diversification of Enterovirus A. Deep mutational scanning of Enterovirus A71 maps and quantifies the impact of genomic insertions, deletions and substitutions on virus fitness and highlights the role of insertions and deletions in the diversification of RNA viruses.
{"title":"Deep mutation, insertion and deletion scanning across the Enterovirus A proteome reveals constraints shaping viral evolution","authors":"William Bakhache, Walker Symonds-Orr, Lauren McCormick, Patrick T. Dolan","doi":"10.1038/s41564-024-01871-y","DOIUrl":"10.1038/s41564-024-01871-y","url":null,"abstract":"Insertions and deletions (InDels) are essential to protein evolution. In RNA viruses, InDels contribute to the emergence of viruses with new phenotypes, including altered host engagement and tropism. However, the tolerance of viral proteins for InDels has not been extensively studied. Here, we conduct deep mutational scanning to map and quantify the mutational tolerance of a complete viral proteome to insertion, deletion and substitution. We engineered approximately 45,000 insertions, 6,000 deletions and 41,000 amino acid substitutions across the nearly 2,200 coding positions of the Enterovirus A71 proteome, quantifying their effects on viral fitness by population sequencing. The vast majority of InDels are lethal to the virus, tolerated at only a few hotspots. Some of these hotspots overlap with sites of host recognition and immune engagement, suggesting tolerance at these sites reflects the important role InDels have played in the past phenotypic diversification of Enterovirus A. Deep mutational scanning of Enterovirus A71 maps and quantifies the impact of genomic insertions, deletions and substitutions on virus fitness and highlights the role of insertions and deletions in the diversification of RNA viruses.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"10 1","pages":"158-168"},"PeriodicalIF":20.5,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41564-024-01871-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142735587","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}
Pub Date : 2024-11-27DOI: 10.1038/s41564-024-01880-x
We look back at this year’s Nature Microbiology content covering the spectrum of microbiology, from fundamental advances to those that aim to tackle pressing concerns facing human health, the environment and the climate.
{"title":"A year of microbiology","authors":"","doi":"10.1038/s41564-024-01880-x","DOIUrl":"10.1038/s41564-024-01880-x","url":null,"abstract":"We look back at this year’s Nature Microbiology content covering the spectrum of microbiology, from fundamental advances to those that aim to tackle pressing concerns facing human health, the environment and the climate.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"9 12","pages":"3079-3080"},"PeriodicalIF":20.5,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41564-024-01880-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142718286","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}
Pub Date : 2024-11-27DOI: 10.1038/s41564-024-01856-x
Nicola Procházková, Martin F. Laursen, Giorgia La Barbera, Eirini Tsekitsidi, Malte S. Jørgensen, Morten A. Rasmussen, Jeroen Raes, Tine R. Licht, Lars O. Dragsted, Henrik M. Roager
The human gut microbiome is highly personal. However, the contribution of gut physiology and environment to variations in the gut microbiome remains understudied. Here we performed an observational trial using multi-omics to profile microbiome composition and metabolism in 61 healthy adults for 9 consecutive days. We assessed day-to-day changes in gut environmental factors and measured whole-gut and segmental intestinal transit time and pH using a wireless motility capsule in a subset of 50 individuals. We observed substantial daily fluctuations, with intra-individual variations in gut microbiome and metabolism associated with changes in stool moisture and faecal pH, and inter-individual variations accounted for by whole-gut and segmental transit times and pH. Metabolites derived from microbial carbohydrate fermentation correlated negatively with the gut passage time and pH, while proteolytic metabolites and breath methane showed a positive correlation. Finally, we identified associations between segmental transit time/pH and coffee-, diet-, host- and microbial-derived metabolites. Our work suggests that gut physiology and environment are key to understanding the individuality of the human gut microbial composition and metabolism. An observational longitudinal clinical trial, incorporating a SmartPill and metabolomics, reveals the role of host factors in shaping the gut microbiome in healthy human adults.
{"title":"Gut physiology and environment explain variations in human gut microbiome composition and metabolism","authors":"Nicola Procházková, Martin F. Laursen, Giorgia La Barbera, Eirini Tsekitsidi, Malte S. Jørgensen, Morten A. Rasmussen, Jeroen Raes, Tine R. Licht, Lars O. Dragsted, Henrik M. Roager","doi":"10.1038/s41564-024-01856-x","DOIUrl":"10.1038/s41564-024-01856-x","url":null,"abstract":"The human gut microbiome is highly personal. However, the contribution of gut physiology and environment to variations in the gut microbiome remains understudied. Here we performed an observational trial using multi-omics to profile microbiome composition and metabolism in 61 healthy adults for 9 consecutive days. We assessed day-to-day changes in gut environmental factors and measured whole-gut and segmental intestinal transit time and pH using a wireless motility capsule in a subset of 50 individuals. We observed substantial daily fluctuations, with intra-individual variations in gut microbiome and metabolism associated with changes in stool moisture and faecal pH, and inter-individual variations accounted for by whole-gut and segmental transit times and pH. Metabolites derived from microbial carbohydrate fermentation correlated negatively with the gut passage time and pH, while proteolytic metabolites and breath methane showed a positive correlation. Finally, we identified associations between segmental transit time/pH and coffee-, diet-, host- and microbial-derived metabolites. Our work suggests that gut physiology and environment are key to understanding the individuality of the human gut microbial composition and metabolism. An observational longitudinal clinical trial, incorporating a SmartPill and metabolomics, reveals the role of host factors in shaping the gut microbiome in healthy human adults.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"9 12","pages":"3210-3225"},"PeriodicalIF":20.5,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41564-024-01856-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142718340","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}
Pub Date : 2024-11-26DOI: 10.1038/s41564-024-01850-3
Matthias Huelsmann, Olga T. Schubert, Martin Ackermann
Microbiome metabolism underlies numerous vital ecosystem functions. Individual microbiome members often perform partial catabolism of substrates or do not express all of the metabolic functions required for growth. Microbiome members can complement each other by exchanging metabolic intermediates and cellular building blocks to achieve a collective metabolism. We currently lack a mechanistic framework to explain why microbiome members adopt partial metabolism and how metabolic functions are distributed among them. Here we argue that natural selection for proteome efficiency—that is, performing essential metabolic fluxes at a minimal protein investment—explains partial metabolism of microbiome members, which underpins the collective metabolism of microbiomes. Using the carbon cycle as an example, we discuss motifs of collective metabolism, the conditions under which these motifs increase the proteome efficiency of individuals and the metabolic interactions they result in. In summary, we propose a mechanistic framework for how collective metabolic functions emerge from selection on individuals. This Perspective explores why microbiome members perform partial metabolism of substrates and suggests that proteome efficiency is a driver of collective microbiome metabolism.
{"title":"A framework for understanding collective microbiome metabolism","authors":"Matthias Huelsmann, Olga T. Schubert, Martin Ackermann","doi":"10.1038/s41564-024-01850-3","DOIUrl":"10.1038/s41564-024-01850-3","url":null,"abstract":"Microbiome metabolism underlies numerous vital ecosystem functions. Individual microbiome members often perform partial catabolism of substrates or do not express all of the metabolic functions required for growth. Microbiome members can complement each other by exchanging metabolic intermediates and cellular building blocks to achieve a collective metabolism. We currently lack a mechanistic framework to explain why microbiome members adopt partial metabolism and how metabolic functions are distributed among them. Here we argue that natural selection for proteome efficiency—that is, performing essential metabolic fluxes at a minimal protein investment—explains partial metabolism of microbiome members, which underpins the collective metabolism of microbiomes. Using the carbon cycle as an example, we discuss motifs of collective metabolism, the conditions under which these motifs increase the proteome efficiency of individuals and the metabolic interactions they result in. In summary, we propose a mechanistic framework for how collective metabolic functions emerge from selection on individuals. This Perspective explores why microbiome members perform partial metabolism of substrates and suggests that proteome efficiency is a driver of collective microbiome metabolism.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"9 12","pages":"3097-3109"},"PeriodicalIF":20.5,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142712443","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}
Pub Date : 2024-11-22DOI: 10.1038/s41564-024-01859-8
Lukas Hafner, Enzo Gadin, Lei Huang, Arthur Frouin, Fabien Laporte, Charlotte Gaultier, Afonso Vieira, Claire Maudet, Hugo Varet, Alexandra Moura, Hélène Bracq-Dieye, Nathalie Tessaud-Rita, Mylène Maury, Melody Dazas, Rachel Legendre, Pauline Gastineau, Yu-Huan Tsai, Jean-Yves Coppée, Caroline Charlier, Etienne Patin, Rayan Chikhi, Eduardo P. C. Rocha, Alexandre Leclercq, Olivier Disson, Hugues Aschard, Marc Lecuit
Microbial pathogenesis is mediated by the expression of virulence genes. However, as microbes with identical virulence gene content can differ in their pathogenic potential, other virulence determinants must be involved. Here, by combining comparative genomics and transcriptomics of a large collection of isolates of the model pathogen Listeria monocytogenes, time-lapse microscopy, in vitro evolution and in vivo experiments, we show that the individual stress responsiveness of L. monocytogenes isolates determines their respective levels of virulence in vivo and reflects their degree of host adaptation. The transcriptional signature that accounts for the heterogeneity in the virulence of L. monocytogenes species is mediated by the stress response regulator SigB and driven by differential stress responsiveness. The tuning of SigB pathway responsiveness is polygenic and influenced by multiple, individually rare gene variations. This study reveals an overarching determinant of microbial virulence, challenging the paradigm of accessory virulence gene content as the major determinant of intraspecies virulence heterogeneity. Differences in virulence across the Listeria monocytogenes species are determined by the fine-tuning of SigB pathway responsiveness and reflect host adaptation.
{"title":"Differential stress responsiveness determines intraspecies virulence heterogeneity and host adaptation in Listeria monocytogenes","authors":"Lukas Hafner, Enzo Gadin, Lei Huang, Arthur Frouin, Fabien Laporte, Charlotte Gaultier, Afonso Vieira, Claire Maudet, Hugo Varet, Alexandra Moura, Hélène Bracq-Dieye, Nathalie Tessaud-Rita, Mylène Maury, Melody Dazas, Rachel Legendre, Pauline Gastineau, Yu-Huan Tsai, Jean-Yves Coppée, Caroline Charlier, Etienne Patin, Rayan Chikhi, Eduardo P. C. Rocha, Alexandre Leclercq, Olivier Disson, Hugues Aschard, Marc Lecuit","doi":"10.1038/s41564-024-01859-8","DOIUrl":"10.1038/s41564-024-01859-8","url":null,"abstract":"Microbial pathogenesis is mediated by the expression of virulence genes. However, as microbes with identical virulence gene content can differ in their pathogenic potential, other virulence determinants must be involved. Here, by combining comparative genomics and transcriptomics of a large collection of isolates of the model pathogen Listeria monocytogenes, time-lapse microscopy, in vitro evolution and in vivo experiments, we show that the individual stress responsiveness of L. monocytogenes isolates determines their respective levels of virulence in vivo and reflects their degree of host adaptation. The transcriptional signature that accounts for the heterogeneity in the virulence of L. monocytogenes species is mediated by the stress response regulator SigB and driven by differential stress responsiveness. The tuning of SigB pathway responsiveness is polygenic and influenced by multiple, individually rare gene variations. This study reveals an overarching determinant of microbial virulence, challenging the paradigm of accessory virulence gene content as the major determinant of intraspecies virulence heterogeneity. Differences in virulence across the Listeria monocytogenes species are determined by the fine-tuning of SigB pathway responsiveness and reflect host adaptation.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"9 12","pages":"3345-3361"},"PeriodicalIF":20.5,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142684161","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}
Pub Date : 2024-11-22DOI: 10.1038/s41564-024-01863-y
Jan Homolak, Lara Berg, Lisa Maier
Entacapone, a drug used in the treatment of Parkinson’s disease, disrupts gut microbial communities by sequestering iron, creating a competitive advantage for iron-scavenging microbes that often carry antimicrobial resistance and virulence genes.
{"title":"Parkinson’s drug starves gut microbes of iron","authors":"Jan Homolak, Lara Berg, Lisa Maier","doi":"10.1038/s41564-024-01863-y","DOIUrl":"10.1038/s41564-024-01863-y","url":null,"abstract":"Entacapone, a drug used in the treatment of Parkinson’s disease, disrupts gut microbial communities by sequestering iron, creating a competitive advantage for iron-scavenging microbes that often carry antimicrobial resistance and virulence genes.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"9 12","pages":"3090-3092"},"PeriodicalIF":20.5,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142684160","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}
Pub Date : 2024-11-22DOI: 10.1038/s41564-024-01855-y
Harshad Ingle, Jerome M. Molleston, Paige D. Hall, Duyen Bui, Leran Wang, Karan D. Bhatt, Lynne Foster, Avan Antia, Siyuan Ding, Sanghyun Lee, Daved H. Fremont, Megan T. Baldridge
Human astroviruses (HAstV) are major causes of gastroenteritis, especially in children, and there are no vaccines or antivirals currently available. Little is known about host factors required for their cellular entry. Here we utilized complementary CRISPR-Cas9-based knockout and activation screens to identify neonatal Fc receptor (FcRn) and dipeptidyl-peptidase IV (DPP4) as entry factors for HAstV infection in vitro. Disruption of FcRn or DPP4 reduced HAstV infection in permissive cells and, reciprocally, overexpression of these factors in non-permissive cells was sufficient to promote infection. We observed direct binding of FcRn, but not DPP4, with HAstV virions and the purified spike protein. This suggests that FcRn is a receptor for HAstVs while DPP4 is a cofactor for entry. Inhibitors for DPP4 and FcRn currently in clinical use prevented HAstV infection in cell lines and human enteroids. Our results reveal mechanisms of HAstV entry as well as druggable targets to limit HAstV infection. A CRISPR-based screen identifies neonatal Fc receptor (FcRn) and dipeptidyl-peptidase IV (DPP4) as entry factors for human astrovirus, and targeting them using available therapies effectively prevents infection in human enteroid cultures.
{"title":"The neonatal Fc receptor is a cellular receptor for human astrovirus","authors":"Harshad Ingle, Jerome M. Molleston, Paige D. Hall, Duyen Bui, Leran Wang, Karan D. Bhatt, Lynne Foster, Avan Antia, Siyuan Ding, Sanghyun Lee, Daved H. Fremont, Megan T. Baldridge","doi":"10.1038/s41564-024-01855-y","DOIUrl":"10.1038/s41564-024-01855-y","url":null,"abstract":"Human astroviruses (HAstV) are major causes of gastroenteritis, especially in children, and there are no vaccines or antivirals currently available. Little is known about host factors required for their cellular entry. Here we utilized complementary CRISPR-Cas9-based knockout and activation screens to identify neonatal Fc receptor (FcRn) and dipeptidyl-peptidase IV (DPP4) as entry factors for HAstV infection in vitro. Disruption of FcRn or DPP4 reduced HAstV infection in permissive cells and, reciprocally, overexpression of these factors in non-permissive cells was sufficient to promote infection. We observed direct binding of FcRn, but not DPP4, with HAstV virions and the purified spike protein. This suggests that FcRn is a receptor for HAstVs while DPP4 is a cofactor for entry. Inhibitors for DPP4 and FcRn currently in clinical use prevented HAstV infection in cell lines and human enteroids. Our results reveal mechanisms of HAstV entry as well as druggable targets to limit HAstV infection. A CRISPR-based screen identifies neonatal Fc receptor (FcRn) and dipeptidyl-peptidase IV (DPP4) as entry factors for human astrovirus, and targeting them using available therapies effectively prevents infection in human enteroid cultures.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"9 12","pages":"3321-3331"},"PeriodicalIF":20.5,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142684162","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}
Pub Date : 2024-11-21DOI: 10.1038/s41564-024-01853-0
Fátima C. Pereira, Xiaowei Ge, Jannie M. Kristensen, Rasmus H. Kirkegaard, Klara Maritsch, Dávid Szamosvári, Stefanie Imminger, David Seki, Juwairiyah B. Shazzad, Yifan Zhu, Marie Decorte, Bela Hausmann, David Berry, Kenneth Wasmund, Arno Schintlmeister, Thomas Böttcher, Ji-Xin Cheng, Michael Wagner
Many human-targeted drugs alter the gut microbiome, leading to implications for host health. However, the mechanisms underlying these effects are not well known. Here we combined quantitative microbiome profiling, long-read metagenomics, stable isotope probing and single-cell chemical imaging to investigate the impact of two widely prescribed drugs on the gut microbiome. Physiologically relevant concentrations of entacapone, a treatment for Parkinson’s disease, or loxapine succinate, used to treat schizophrenia, were incubated ex vivo with human faecal samples. Both drugs significantly impact microbial activity, more so than microbial abundance. Mechanistically, entacapone can complex and deplete available iron resulting in gut microbiome composition and function changes. Microbial growth can be rescued by replenishing levels of microbiota-accessible iron. Further, entacapone-induced iron starvation selected for iron-scavenging gut microbiome members encoding antimicrobial resistance and virulence genes. These findings reveal the impact of two under-investigated drugs on whole microbiomes and identify metal sequestration as a mechanism of drug-induced microbiome disturbance. Entacapone, a Parkinson’s disease medication, sequesters iron resulting in a selective inhibition of gut microbial activity.
{"title":"The Parkinson’s disease drug entacapone disrupts gut microbiome homeostasis via iron sequestration","authors":"Fátima C. Pereira, Xiaowei Ge, Jannie M. Kristensen, Rasmus H. Kirkegaard, Klara Maritsch, Dávid Szamosvári, Stefanie Imminger, David Seki, Juwairiyah B. Shazzad, Yifan Zhu, Marie Decorte, Bela Hausmann, David Berry, Kenneth Wasmund, Arno Schintlmeister, Thomas Böttcher, Ji-Xin Cheng, Michael Wagner","doi":"10.1038/s41564-024-01853-0","DOIUrl":"10.1038/s41564-024-01853-0","url":null,"abstract":"Many human-targeted drugs alter the gut microbiome, leading to implications for host health. However, the mechanisms underlying these effects are not well known. Here we combined quantitative microbiome profiling, long-read metagenomics, stable isotope probing and single-cell chemical imaging to investigate the impact of two widely prescribed drugs on the gut microbiome. Physiologically relevant concentrations of entacapone, a treatment for Parkinson’s disease, or loxapine succinate, used to treat schizophrenia, were incubated ex vivo with human faecal samples. Both drugs significantly impact microbial activity, more so than microbial abundance. Mechanistically, entacapone can complex and deplete available iron resulting in gut microbiome composition and function changes. Microbial growth can be rescued by replenishing levels of microbiota-accessible iron. Further, entacapone-induced iron starvation selected for iron-scavenging gut microbiome members encoding antimicrobial resistance and virulence genes. These findings reveal the impact of two under-investigated drugs on whole microbiomes and identify metal sequestration as a mechanism of drug-induced microbiome disturbance. Entacapone, a Parkinson’s disease medication, sequesters iron resulting in a selective inhibition of gut microbial activity.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"9 12","pages":"3165-3183"},"PeriodicalIF":20.5,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41564-024-01853-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142678277","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}
Pub Date : 2024-11-20DOI: 10.1038/s41564-024-01866-9
Masaru K. Nobu
Multiple histories converge in Masaru Nobu’s story of culturing an archaeon closely related to us eukaryotes.
Masaru Nobu 讲述了培养一种与我们真核生物密切相关的古生物的故事。
{"title":"Engineering history with Asgard archaea of the kingdom Promethearchaeati","authors":"Masaru K. Nobu","doi":"10.1038/s41564-024-01866-9","DOIUrl":"10.1038/s41564-024-01866-9","url":null,"abstract":"Multiple histories converge in Masaru Nobu’s story of culturing an archaeon closely related to us eukaryotes.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"9 12","pages":"3086-3087"},"PeriodicalIF":20.5,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142673236","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}
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