Pub Date : 2023-10-02DOI: 10.1038/d41587-023-00013-9
Laura DeFrancesco
{"title":"Cartography Biosciences and Nested Therapeutics: Diamonds in the rough.","authors":"Laura DeFrancesco","doi":"10.1038/d41587-023-00013-9","DOIUrl":"10.1038/d41587-023-00013-9","url":null,"abstract":"","PeriodicalId":19084,"journal":{"name":"Nature biotechnology","volume":" ","pages":""},"PeriodicalIF":46.9,"publicationDate":"2023-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41143505","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 : 2023-10-02DOI: 10.1038/s41587-023-01955-w
Benjamin J. Leslie, Benjamin Lang, M. Madan Babu
Transcription factors containing disordered regions can now be mapped across the genome, aiding functional studies.
含有紊乱区域的转录因子现在可以在整个基因组中进行映射，从而有助于功能研究。
{"title":"A genome-wide view of disordered proteins","authors":"Benjamin J. Leslie, Benjamin Lang, M. Madan Babu","doi":"10.1038/s41587-023-01955-w","DOIUrl":"10.1038/s41587-023-01955-w","url":null,"abstract":"Transcription factors containing disordered regions can now be mapped across the genome, aiding functional studies.","PeriodicalId":19084,"journal":{"name":"Nature biotechnology","volume":"42 1","pages":"32-34"},"PeriodicalIF":46.9,"publicationDate":"2023-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41129002","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 : 2023-10-02DOI: 10.1038/s41587-023-02005-1
Decentralized autonomous organizations are growing as alternative research funding models, but are also strong scientific communities. We should get on board.
分散式自治组织作为另一种研究资助模式正在发展壮大，同时也是强大的科学社区。我们应该加入其中。
{"title":"The community of the DAO","authors":"","doi":"10.1038/s41587-023-02005-1","DOIUrl":"10.1038/s41587-023-02005-1","url":null,"abstract":"Decentralized autonomous organizations are growing as alternative research funding models, but are also strong scientific communities. We should get on board.","PeriodicalId":19084,"journal":{"name":"Nature biotechnology","volume":"41 10","pages":"1357-1357"},"PeriodicalIF":46.9,"publicationDate":"2023-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41587-023-02005-1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41138014","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 : 2023-09-26DOI: 10.1038/s41587-023-01992-5
Claire Turrell
Food tech companies are taking bacteria that capture CO2 from air to make edible and nutritious food and drink.
食品科技公司正在利用能从空气中捕捉二氧化碳的细菌来制作可食用的营养食品和饮料。
{"title":"From air to your plate: tech startups making food from atmospheric CO2","authors":"Claire Turrell","doi":"10.1038/s41587-023-01992-5","DOIUrl":"10.1038/s41587-023-01992-5","url":null,"abstract":"Food tech companies are taking bacteria that capture CO2 from air to make edible and nutritious food and drink.","PeriodicalId":19084,"journal":{"name":"Nature biotechnology","volume":"41 10","pages":"1362-1364"},"PeriodicalIF":46.9,"publicationDate":"2023-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41142603","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 : 2023-09-25DOI: 10.1038/s41587-023-01948-9
Zihan Xu, Andras Sziraki, Jasper Lee, Wei Zhou, Junyue Cao
We present a combinatorial indexing method, PerturbSci-Kinetics, for capturing whole transcriptomes, nascent transcriptomes and single guide RNA (sgRNA) identities across hundreds of genetic perturbations at the single-cell level. Profiling a pooled CRISPR screen targeting various biological processes, we show the gene expression regulation during RNA synthesis, processing and degradation, miRNA biogenesis and mitochondrial mRNA processing, systematically decoding the genome-wide regulatory network that underlies RNA temporal dynamics at scale. mRNA kinetics are described by combining single-cell combinatorial indexing with metabolic labeling and pooled CRISPR screens.
{"title":"Dissecting key regulators of transcriptome kinetics through scalable single-cell RNA profiling of pooled CRISPR screens","authors":"Zihan Xu, Andras Sziraki, Jasper Lee, Wei Zhou, Junyue Cao","doi":"10.1038/s41587-023-01948-9","DOIUrl":"10.1038/s41587-023-01948-9","url":null,"abstract":"We present a combinatorial indexing method, PerturbSci-Kinetics, for capturing whole transcriptomes, nascent transcriptomes and single guide RNA (sgRNA) identities across hundreds of genetic perturbations at the single-cell level. Profiling a pooled CRISPR screen targeting various biological processes, we show the gene expression regulation during RNA synthesis, processing and degradation, miRNA biogenesis and mitochondrial mRNA processing, systematically decoding the genome-wide regulatory network that underlies RNA temporal dynamics at scale. mRNA kinetics are described by combining single-cell combinatorial indexing with metabolic labeling and pooled CRISPR screens.","PeriodicalId":19084,"journal":{"name":"Nature biotechnology","volume":"42 8","pages":"1218-1223"},"PeriodicalIF":33.1,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10961254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41128363","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 : 2023-09-25DOI: 10.1038/s41587-023-01931-4
Kunal Jindal, Mohd Tayyab Adil, Naoto Yamaguchi, Xue Yang, Helen C. Wang, Kenji Kamimoto, Guillermo C. Rivera-Gonzalez, Samantha A. Morris
Complex gene regulatory mechanisms underlie differentiation and reprogramming. Contemporary single-cell lineage-tracing (scLT) methods use expressed, heritable DNA barcodes to combine cell lineage readout with single-cell transcriptomics. However, reliance on transcriptional profiling limits adaptation to other single-cell assays. With CellTag-multi, we present an approach that enables direct capture of heritable random barcodes expressed as polyadenylated transcripts, in both single-cell RNA sequencing and single-cell Assay for Transposase Accessible Chromatin using sequencing assays, allowing for independent clonal tracking of transcriptional and epigenomic cell states. We validate CellTag-multi to characterize progenitor cell lineage priming during mouse hematopoiesis. Additionally, in direct reprogramming of fibroblasts to endoderm progenitors, we identify core regulatory programs underlying on-target and off-target fates. Furthermore, we reveal the transcription factor Zfp281 as a regulator of reprogramming outcome, biasing cells toward an off-target mesenchymal fate. Our results establish CellTag-multi as a lineage-tracing method compatible with multiple single-cell modalities and demonstrate its utility in revealing fate-specifying gene regulatory changes across diverse paradigms of differentiation and reprogramming. Lineage tracing using both transcriptomics and chromatin accessibility provides mechanistic insights into cell fate.
{"title":"Single-cell lineage capture across genomic modalities with CellTag-multi reveals fate-specific gene regulatory changes","authors":"Kunal Jindal, Mohd Tayyab Adil, Naoto Yamaguchi, Xue Yang, Helen C. Wang, Kenji Kamimoto, Guillermo C. Rivera-Gonzalez, Samantha A. Morris","doi":"10.1038/s41587-023-01931-4","DOIUrl":"10.1038/s41587-023-01931-4","url":null,"abstract":"Complex gene regulatory mechanisms underlie differentiation and reprogramming. Contemporary single-cell lineage-tracing (scLT) methods use expressed, heritable DNA barcodes to combine cell lineage readout with single-cell transcriptomics. However, reliance on transcriptional profiling limits adaptation to other single-cell assays. With CellTag-multi, we present an approach that enables direct capture of heritable random barcodes expressed as polyadenylated transcripts, in both single-cell RNA sequencing and single-cell Assay for Transposase Accessible Chromatin using sequencing assays, allowing for independent clonal tracking of transcriptional and epigenomic cell states. We validate CellTag-multi to characterize progenitor cell lineage priming during mouse hematopoiesis. Additionally, in direct reprogramming of fibroblasts to endoderm progenitors, we identify core regulatory programs underlying on-target and off-target fates. Furthermore, we reveal the transcription factor Zfp281 as a regulator of reprogramming outcome, biasing cells toward an off-target mesenchymal fate. Our results establish CellTag-multi as a lineage-tracing method compatible with multiple single-cell modalities and demonstrate its utility in revealing fate-specifying gene regulatory changes across diverse paradigms of differentiation and reprogramming. Lineage tracing using both transcriptomics and chromatin accessibility provides mechanistic insights into cell fate.","PeriodicalId":19084,"journal":{"name":"Nature biotechnology","volume":"42 6","pages":"946-959"},"PeriodicalIF":46.9,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11180607/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41142721","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 : 2023-09-25DOI: 10.1038/s41587-023-01957-8
Menglin Wang, Benoit Rousseau, Kunyu Qiu, Guannan Huang, Yu Zhang, Hang Su, Christine Le Bihan-Benjamin, Ines Khati, Oliver Artz, Michael B. Foote, Yung-Yi Cheng, Kuo-Hsiung Lee, Michael Z. Miao, Yue Sun, Philippe-Jean Bousquet, Marc Hilmi, Elise Dumas, Anne-Sophie Hamy, Fabien Reyal, Lin Lin, Paul M. Armistead, Wantong Song, Ava Vargason, Janelle C. Arthur, Yun Liu, Jianfeng Guo, Xuefei Zhou, Juliane Nguyen, Yongqun He, Jenny P.-Y. Ting, Aaron C. Anselmo, Leaf Huang
Increasing evidence implicates the tumor microbiota as a factor that can influence cancer progression. In patients with colorectal cancer (CRC), we found that pre-resection antibiotics targeting anaerobic bacteria substantially improved disease-free survival by 25.5%. For mouse studies, we designed an antibiotic silver-tinidazole complex encapsulated in liposomes (LipoAgTNZ) to eliminate tumor-associated bacteria in the primary tumor and liver metastases without causing gut microbiome dysbiosis. Mouse CRC models colonized by tumor-promoting bacteria (Fusobacterium nucleatum spp.) or probiotics (Escherichia coli Nissle spp.) responded to LipoAgTNZ therapy, which enabled more than 70% long-term survival in two F. nucleatum-infected CRC models. The antibiotic treatment generated microbial neoantigens that elicited anti-tumor CD8+ T cells. Heterologous and homologous bacterial epitopes contributed to the immunogenicity, priming T cells to recognize both infected and uninfected tumors. Our strategy targets tumor-associated bacteria to elicit anti-tumoral immunity, paving the way for microbiome–immunotherapy interventions. Killing bacteria in tumors boosts survival in a mouse model of colon cancer.
{"title":"Killing tumor-associated bacteria with a liposomal antibiotic generates neoantigens that induce anti-tumor immune responses","authors":"Menglin Wang, Benoit Rousseau, Kunyu Qiu, Guannan Huang, Yu Zhang, Hang Su, Christine Le Bihan-Benjamin, Ines Khati, Oliver Artz, Michael B. Foote, Yung-Yi Cheng, Kuo-Hsiung Lee, Michael Z. Miao, Yue Sun, Philippe-Jean Bousquet, Marc Hilmi, Elise Dumas, Anne-Sophie Hamy, Fabien Reyal, Lin Lin, Paul M. Armistead, Wantong Song, Ava Vargason, Janelle C. Arthur, Yun Liu, Jianfeng Guo, Xuefei Zhou, Juliane Nguyen, Yongqun He, Jenny P.-Y. Ting, Aaron C. Anselmo, Leaf Huang","doi":"10.1038/s41587-023-01957-8","DOIUrl":"10.1038/s41587-023-01957-8","url":null,"abstract":"Increasing evidence implicates the tumor microbiota as a factor that can influence cancer progression. In patients with colorectal cancer (CRC), we found that pre-resection antibiotics targeting anaerobic bacteria substantially improved disease-free survival by 25.5%. For mouse studies, we designed an antibiotic silver-tinidazole complex encapsulated in liposomes (LipoAgTNZ) to eliminate tumor-associated bacteria in the primary tumor and liver metastases without causing gut microbiome dysbiosis. Mouse CRC models colonized by tumor-promoting bacteria (Fusobacterium nucleatum spp.) or probiotics (Escherichia coli Nissle spp.) responded to LipoAgTNZ therapy, which enabled more than 70% long-term survival in two F. nucleatum-infected CRC models. The antibiotic treatment generated microbial neoantigens that elicited anti-tumor CD8+ T cells. Heterologous and homologous bacterial epitopes contributed to the immunogenicity, priming T cells to recognize both infected and uninfected tumors. Our strategy targets tumor-associated bacteria to elicit anti-tumoral immunity, paving the way for microbiome–immunotherapy interventions. Killing bacteria in tumors boosts survival in a mouse model of colon cancer.","PeriodicalId":19084,"journal":{"name":"Nature biotechnology","volume":"42 8","pages":"1263-1274"},"PeriodicalIF":33.1,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41160150","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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