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Species: human
Number of cells: 93218
Study size: 2GB

Immunology 
immuno-oncology 
Ovary 
Ovarian cancer 
Ligand-receptor 

Single-cell dissection of cellular components and interactions shaping the tumor immune phenotypes in ovarian cancer (All)

Milena Hornburg, Mélanie Desbois, Shan Lu, Yinghui Guan, Amy A.Lo, Susan Kaufman, Ashley Elrod, Alina Lotstein, Teresa M.DesRochers, Jose L.Munoz-Rodriguez, Xingwei Wang, Jennifer Giltnane, Oleg Mayba, Shannon J.Turley, Richard Bourgon, Anneleen Daemen, Yulei Wang

Distinct T cell infiltration patterns, i.e., immune infiltrated, excluded, and desert, result in different responses to cancer immunotherapies. However, the key determinants and biology underpinning these tumor immune phenotypes remain elusive. Here, we provide a high-resolution dissection of the entire tumor ecosystem through single-cell RNA-sequencing analysis of 15 ovarian tumors. Immune-desert tumors are characterized by unique tumor cell-intrinsic features, including metabolic pathways and low antigen presentation, and an enrichment of monocytes and immature macrophages. Immune-infiltrated and -excluded tumors differ markedly in their T cell composition and fibroblast subsets. Furthermore, our study reveals chemokine receptor-ligand interactions within and across compartments as potential mechanisms mediating immune cell infiltration, exemplified by the tumor cell-T cell cross talk via CXCL16-CXCR6 and stromal-immune cell cross talk via CXCL12/14-CXCR4. Our data highlight potential molecular mechanisms that shape the tumor immune phenotypes and may inform therapeutic strategies to improve clinical benefit from cancer immunotherapies.

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Species: human
Number of cells: 16872
Study size: 200MB

Immunology 
immuno-oncology 
Ovary 
Ovarian cancer 
Ligand-receptor 

Single-cell dissection of cellular components and interactions shaping the tumor immune phenotypes in ovarian cancer (T and NK)

Milena Hornburg, Mélanie Desbois, Shan Lu, Yinghui Guan, Amy A.Lo, Susan Kaufman, Ashley Elrod, Alina Lotstein, Teresa M.DesRochers, Jose L.Munoz-Rodriguez, Xingwei Wang, Jennifer Giltnane, Oleg Mayba, Shannon J.Turley, Richard Bourgon, Anneleen Daemen, Yulei Wang

Distinct T cell infiltration patterns, i.e., immune infiltrated, excluded, and desert, result in different responses to cancer immunotherapies. However, the key determinants and biology underpinning these tumor immune phenotypes remain elusive. Here, we provide a high-resolution dissection of the entire tumor ecosystem through single-cell RNA-sequencing analysis of 15 ovarian tumors. Immune-desert tumors are characterized by unique tumor cell-intrinsic features, including metabolic pathways and low antigen presentation, and an enrichment of monocytes and immature macrophages. Immune-infiltrated and -excluded tumors differ markedly in their T cell composition and fibroblast subsets. Furthermore, our study reveals chemokine receptor-ligand interactions within and across compartments as potential mechanisms mediating immune cell infiltration, exemplified by the tumor cell-T cell cross talk via CXCL16-CXCR6 and stromal-immune cell cross talk via CXCL12/14-CXCR4. Our data highlight potential molecular mechanisms that shape the tumor immune phenotypes and may inform therapeutic strategies to improve clinical benefit from cancer immunotherapies.

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Species: human
Number of cells: 9885
Study size: 300MB

Immunology 
immuno-oncology 
Ovary 
Ovarian cancer 
Ligand-receptor 

Single-cell dissection of cellular components and interactions shaping the tumor immune phenotypes in ovarian cancer (Fibroblast)

Milena Hornburg, Mélanie Desbois, Shan Lu, Yinghui Guan, Amy A.Lo, Susan Kaufman, Ashley Elrod, Alina Lotstein, Teresa M.DesRochers, Jose L.Munoz-Rodriguez, Xingwei Wang, Jennifer Giltnane, Oleg Mayba, Shannon J.Turley, Richard Bourgon, Anneleen Daemen, Yulei Wang

Distinct T cell infiltration patterns, i.e., immune infiltrated, excluded, and desert, result in different responses to cancer immunotherapies. However, the key determinants and biology underpinning these tumor immune phenotypes remain elusive. Here, we provide a high-resolution dissection of the entire tumor ecosystem through single-cell RNA-sequencing analysis of 15 ovarian tumors. Immune-desert tumors are characterized by unique tumor cell-intrinsic features, including metabolic pathways and low antigen presentation, and an enrichment of monocytes and immature macrophages. Immune-infiltrated and -excluded tumors differ markedly in their T cell composition and fibroblast subsets. Furthermore, our study reveals chemokine receptor-ligand interactions within and across compartments as potential mechanisms mediating immune cell infiltration, exemplified by the tumor cell-T cell cross talk via CXCL16-CXCR6 and stromal-immune cell cross talk via CXCL12/14-CXCR4. Our data highlight potential molecular mechanisms that shape the tumor immune phenotypes and may inform therapeutic strategies to improve clinical benefit from cancer immunotherapies.

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Species: human
Number of cells: 13123
Study size: 254MB

Immunology 
immuno-oncology 
Ovary 
Ovarian cancer 
Ligand-receptor 

Single-cell dissection of cellular components and interactions shaping the tumor immune phenotypes in ovarian cancer (Myeloid)

Milena Hornburg, Mélanie Desbois, Shan Lu, Yinghui Guan, Amy A.Lo, Susan Kaufman, Ashley Elrod, Alina Lotstein, Teresa M.DesRochers, Jose L.Munoz-Rodriguez, Xingwei Wang, Jennifer Giltnane, Oleg Mayba, Shannon J.Turley, Richard Bourgon, Anneleen Daemen, Yulei Wang

Distinct T cell infiltration patterns, i.e., immune infiltrated, excluded, and desert, result in different responses to cancer immunotherapies. However, the key determinants and biology underpinning these tumor immune phenotypes remain elusive. Here, we provide a high-resolution dissection of the entire tumor ecosystem through single-cell RNA-sequencing analysis of 15 ovarian tumors. Immune-desert tumors are characterized by unique tumor cell-intrinsic features, including metabolic pathways and low antigen presentation, and an enrichment of monocytes and immature macrophages. Immune-infiltrated and -excluded tumors differ markedly in their T cell composition and fibroblast subsets. Furthermore, our study reveals chemokine receptor-ligand interactions within and across compartments as potential mechanisms mediating immune cell infiltration, exemplified by the tumor cell-T cell cross talk via CXCL16-CXCR6 and stromal-immune cell cross talk via CXCL12/14-CXCR4. Our data highlight potential molecular mechanisms that shape the tumor immune phenotypes and may inform therapeutic strategies to improve clinical benefit from cancer immunotherapies.

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Species: human
Number of cells: 38658
Study size: 2GB

COVID-19 
Respiratory tract 

COVID-19 severity correlates with airway epithelium–immune cell interactions identified by single-cell analysis (Upper and lower respiratory tract)

Robert Lorenz Chua, Soeren Lukassen, Saskia Trump, Bianca P. Hennig, Daniel Wendisch, Fabian Pott, Olivia Debnath, Loreen Thürmann, Florian Kurth, Maria Theresa Völker, Julia Kazmierski, Bernd Timmermann, Sven Twardziok, Stefan Schneider, Felix Machleidt, Holger Müller-Redetzky, Melanie Maier, Alexander Krannich, Sein Schmidt, Felix Balzer, Johannes Liebig, Jennifer Loske, Norbert Suttorp, Jürgen Eils, Naveed Ishaque, Uwe Gerd Liebert, Christof von Kalle, Andreas Hocke, Martin Witzenrath, Christine Goffinet, Christian Drosten, Sven Laudi, Irina Lehmann, Christian Conrad, Leif-Erik Sander & Roland Eils

To investigate the immune response and mechanisms associated with severe coronavirus disease 2019 (COVID-19), we performed single-cell RNA sequencing on nasopharyngeal and bronchial samples from 19 clinically well-characterized patients with moderate or critical disease and from five healthy controls. We identified airway epithelial cell types and states vulnerable to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In patients with COVID-19, epithelial cells showed an average three-fold increase in expression of the SARS-CoV-2 entry receptor ACE2, which correlated with interferon signals by immune cells. Compared to moderate cases, critical cases exhibited stronger interactions between epithelial and immune cells, as indicated by ligand–receptor expression profiles, and activated immune cells, including inflammatory macrophages expressing CCL2, CCL3, CCL20, CXCL1, CXCL3, CXCL10, IL8, IL1B and TNF. The transcriptional differences in critical cases compared to moderate cases likely contribute to clinical observations of heightened inflammatory tissue damage, lung injury and respiratory failure. Our data suggest that pharmacologic inhibition of the CCR1 and/or CCR5 pathways might suppress immune hyperactivation in critical COVID-19.

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Species: human
Number of cells: 210614
Study size: 2GB

Colon 
ulcerative colitis 

Intra-and inter-cellular rewiring of the human colon during ulcerative colitis (discovery and validation cohorts - immune cell)

Christopher S. Smillie, Moshe Biton, Jose Ordovas-Montanes, Keri M. Sullivan, Grace Burgin, Daniel B. Graham, Rebecca H. Herbst, Noga Rogel, Michal Slyper, Julia Waldman, Malika Sud, Elizabeth Andrews, 8 Gabriella Velonias, Adam L. Haber, Karthik Jagadeesh, Sanja Vickovic, Junmei Yao, Christine Stevens, Danielle Dionne, Lan T. Nguyen, Alexandra-Chloe´ Villani, Matan Hofree, Elizabeth A. Creasey, Hailiang Huang, Orit Rozenblatt-Rosen, John J. Garber, Hamed Khalili, A. Nicole Desch, Mark J. Daly, Ashwin N. Ananthakrishnan, Alex K. Shalek, Ramnik J. Xavier, and Aviv Regev

Genome-wide association studies (GWAS) have revealed risk alleles for ulcerative colitis (UC). To understand their cell type specificities and pathways of action, we generate an atlas of 366,650 cells from the colon mucosa of 18 UC patients and 12 healthy individuals, revealing 51 epithelial, stromal, and immune cell subsets, including BEST4+ enterocytes, microfold-like cells, and IL13RA2+IL11+ inflammatory fibroblasts, which we associate with resistance to anti-TNF treatment. Inflammatory fibroblasts, inflammatory monocytes, microfold-like cells, and T cells that co-express CD8 and IL-17 expand with disease, forming intercellular interaction hubs. Many UC risk genes are cell type specific and co-regulated within relatively few gene modules, suggesting convergence onto limited sets of cell types and pathways. Using this observation, we nominate and infer functions for specific risk genes across GWAS loci. Our work provides a framework for interrogating complex human diseases and mapping risk variants to cell types and pathways.

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Species: human
Number of cells: 31872
Study size: 455MB

Colon 
ulcerative colitis 

Intra-and inter-cellular rewiring of the human colon during ulcerative colitis (discovery and validation cohorts - fibroblast)

Christopher S. Smillie, Moshe Biton, Jose Ordovas-Montanes, Keri M. Sullivan, Grace Burgin, Daniel B. Graham, Rebecca H. Herbst, Noga Rogel, Michal Slyper, Julia Waldman, Malika Sud, Elizabeth Andrews, 8 Gabriella Velonias, Adam L. Haber, Karthik Jagadeesh, Sanja Vickovic, Junmei Yao, Christine Stevens, Danielle Dionne, Lan T. Nguyen, Alexandra-Chloe´ Villani, Matan Hofree, Elizabeth A. Creasey, Hailiang Huang, Orit Rozenblatt-Rosen, John J. Garber, Hamed Khalili, A. Nicole Desch, Mark J. Daly, Ashwin N. Ananthakrishnan, Alex K. Shalek, Ramnik J. Xavier, and Aviv Regev

Genome-wide association studies (GWAS) have revealed risk alleles for ulcerative colitis (UC). To understand their cell type specificities and pathways of action, we generate an atlas of 366,650 cells from the colon mucosa of 18 UC patients and 12 healthy individuals, revealing 51 epithelial, stromal, and immune cell subsets, including BEST4+ enterocytes, microfold-like cells, and IL13RA2+IL11+ inflammatory fibroblasts, which we associate with resistance to anti-TNF treatment. Inflammatory fibroblasts, inflammatory monocytes, microfold-like cells, and T cells that co-express CD8 and IL-17 expand with disease, forming intercellular interaction hubs. Many UC risk genes are cell type specific and co-regulated within relatively few gene modules, suggesting convergence onto limited sets of cell types and pathways. Using this observation, we nominate and infer functions for specific risk genes across GWAS loci. Our work provides a framework for interrogating complex human diseases and mapping risk variants to cell types and pathways.

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Species: human
Number of cells: 123006
Study size: 2GB

Colon 
ulcerative colitis 

Intra-and inter-cellular rewiring of the human colon during ulcerative colitis (discovery and validation cohorts - epithelial cell)

Christopher S. Smillie, Moshe Biton, Jose Ordovas-Montanes, Keri M. Sullivan, Grace Burgin, Daniel B. Graham, Rebecca H. Herbst, Noga Rogel, Michal Slyper, Julia Waldman, Malika Sud, Elizabeth Andrews, 8 Gabriella Velonias, Adam L. Haber, Karthik Jagadeesh, Sanja Vickovic, Junmei Yao, Christine Stevens, Danielle Dionne, Lan T. Nguyen, Alexandra-Chloe´ Villani, Matan Hofree, Elizabeth A. Creasey, Hailiang Huang, Orit Rozenblatt-Rosen, John J. Garber, Hamed Khalili, A. Nicole Desch, Mark J. Daly, Ashwin N. Ananthakrishnan, Alex K. Shalek, Ramnik J. Xavier, and Aviv Regev

Genome-wide association studies (GWAS) have revealed risk alleles for ulcerative colitis (UC). To understand their cell type specificities and pathways of action, we generate an atlas of 366,650 cells from the colon mucosa of 18 UC patients and 12 healthy individuals, revealing 51 epithelial, stromal, and immune cell subsets, including BEST4+ enterocytes, microfold-like cells, and IL13RA2+IL11+ inflammatory fibroblasts, which we associate with resistance to anti-TNF treatment. Inflammatory fibroblasts, inflammatory monocytes, microfold-like cells, and T cells that co-express CD8 and IL-17 expand with disease, forming intercellular interaction hubs. Many UC risk genes are cell type specific and co-regulated within relatively few gene modules, suggesting convergence onto limited sets of cell types and pathways. Using this observation, we nominate and infer functions for specific risk genes across GWAS loci. Our work provides a framework for interrogating complex human diseases and mapping risk variants to cell types and pathways.

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Species: mouse
Number of cells: 26537
Study size: 513MB

Cell development 
retina 

Single-Cell RNA-Seq Analysis of Retinal Development Identifies NFI Factors as Regulating Mitotic Exit and Late-Born Cell Specification (NFI)

Brian S. Clark, Genevieve L. Stein-O’Brien, Fion Shiau, Gabrielle H. Cannon, Emily Davis-Marcisak, Thomas Sherman, Clayton P. Santiago, Thanh V. Hoang, Fatemeh Rajaii, Rebecca E. James-Esposito, Richard M. Gronostajski, Elana J. Fertig, Loyal A. Goff, and Seth Blackshaw

Precise temporal control of gene expression in neuronal progenitors is necessary for correct regulation of neurogenesis and cell fate specification. However, the cellular heterogeneity of the developing CNS has posed a major obstacle to identifying the gene regulatory networks that control these processes. To address this, we used single-cell RNA sequencing to profile ten developmental stages encompassing the full course of retinal neurogenesis. This allowed us to comprehensively characterize changes in gene expression that occur during initiation of neurogenesis, changes in developmental competence, and specification and differentiation of each major retinal cell type. We identify the NFI transcription factors (Nfia, Nfib, and Nfix) as selectively expressed in late retinal progenitor cells and show that they control bipolar interneuron and Müller glia cell fate specification and promote proliferative quiescence.

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Species: mouse
Number of cells: 747
Study size: 66MB

Cell development 
retina 

Single-Cell RNA-Seq Analysis of Retinal Development Identifies NFI Factors as Regulating Mitotic Exit and Late-Born Cell Specification (Smart_Seq2)

Brian S. Clark, Genevieve L. Stein-O’Brien, Fion Shiau, Gabrielle H. Cannon, Emily Davis-Marcisak, Thomas Sherman, Clayton P. Santiago, Thanh V. Hoang, Fatemeh Rajaii, Rebecca E. James-Esposito, Richard M. Gronostajski, Elana J. Fertig, Loyal A. Goff, and Seth Blackshaw

Precise temporal control of gene expression in neuronal progenitors is necessary for correct regulation of neurogenesis and cell fate specification. However, the cellular heterogeneity of the developing CNS has posed a major obstacle to identifying the gene regulatory networks that control these processes. To address this, we used single-cell RNA sequencing to profile ten developmental stages encompassing the full course of retinal neurogenesis. This allowed us to comprehensively characterize changes in gene expression that occur during initiation of neurogenesis, changes in developmental competence, and specification and differentiation of each major retinal cell type. We identify the NFI transcription factors (Nfia, Nfib, and Nfix) as selectively expressed in late retinal progenitor cells and show that they control bipolar interneuron and Müller glia cell fate specification and promote proliferative quiescence.

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Species: human
Number of cells: 7721
Study size: 327MB

Cell development 
Organoid 
Kidney 

In vivo developmental trajectories of human podocyte inform in vitro differentiation of pluripotent stem cell-derived podocytes (Organoid)

Tracy Tran, Nils O. Lindstrom, Andrew Ransick, Guilherme De Sena Brandine, Qiuyu Guo, Albert D. Kim, Balint Der, Janos Peti-Peterdi, Andrew D. Smith, Matthew Thornton, Brendan Grubbs, Jill A. McMahon, and Andrew P. McMahon

The renal corpuscle of the kidney comprises a glomerular vasculature embraced by podocytes and supported by mesangial myofibroblasts, which ensure plasma filtration at the podocyte-generated slit diaphragm. With a spectrum of podocyte-expressed gene mutations causing chronic disease, an enhanced understanding of podocyte development and function to create relevant in vitro podocyte models is a clinical imperative. To characterize podocyte development, scRNA-seq was performed on human fetal kidneys, identifying distinct transcriptional signatures accompanying the differentiation of functional podocytes from progenitors. Interestingly, organoid-generated podocytes exhibited highly similar, progressive transcriptional profiles despite an absence of the vasculature, although abnormal gene expression was pinpointed in late podocytes. On transplantation into mice, organoid-derived podocytes recruited the host vasculature and partially corrected transcriptional profiles. Thus, human podocyte development is mostly intrinsically regulated and vascular interactions refine maturation. These studies support the application of organoid-derived podocytes to model disease and to restore or replace normal kidney functions.

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Species: human
Number of cells: 6139
Study size: 84MB

Cell development 
Kidney 

In vivo developmental trajectories of human podocyte inform in vitro differentiation of pluripotent stem cell-derived podocytes (Week 15)

Tracy Tran, Nils O. Lindstrom, Andrew Ransick, Guilherme De Sena Brandine, Qiuyu Guo, Albert D. Kim, Balint Der, Janos Peti-Peterdi, Andrew D. Smith, Matthew Thornton, Brendan Grubbs, Jill A. McMahon, and Andrew P. McMahon

The renal corpuscle of the kidney comprises a glomerular vasculature embraced by podocytes and supported by mesangial myofibroblasts, which ensure plasma filtration at the podocyte-generated slit diaphragm. With a spectrum of podocyte-expressed gene mutations causing chronic disease, an enhanced understanding of podocyte development and function to create relevant in vitro podocyte models is a clinical imperative. To characterize podocyte development, scRNA-seq was performed on human fetal kidneys, identifying distinct transcriptional signatures accompanying the differentiation of functional podocytes from progenitors. Interestingly, organoid-generated podocytes exhibited highly similar, progressive transcriptional profiles despite an absence of the vasculature, although abnormal gene expression was pinpointed in late podocytes. On transplantation into mice, organoid-derived podocytes recruited the host vasculature and partially corrected transcriptional profiles. Thus, human podocyte development is mostly intrinsically regulated and vascular interactions refine maturation. These studies support the application of organoid-derived podocytes to model disease and to restore or replace normal kidney functions.

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Species: mouse
Number of cells: 250
Study size: 39MB

Cell development 
embryo 
endothelial cell 

A single-cell molecular map of mouse gastrulation and early organogenesis (Smart-seq2 - endothelial cells)

Blanca Pijuan-Sala, Jonathan A. Griffiths, Carolina Guibentif, Tom W. Hiscock, Wajid Jawaid, Fernando J. Calero-Nieto, Carla Mulas, Ximena Ibarra-Soria, Richard C. V. Tyser, Debbie Lee Lian Ho, Wolf Reik, Shankar Srinivas, Benjamin D. Simons, Jennifer Nichols, John C. Marioni, Berthold Gottgens

Across the animal kingdom, gastrulation represents a key developmental event during which embryonic pluripotent cells diversify into lineage-specific precursors that will generate the adult organism. Here we report the transcriptional profiles of 116,312 single cells from mouse embryos collected at nine sequential time points ranging from 6.5 to 8.5 days post-fertilization. We construct a molecular map of cellular differentiation from pluripotency towards all major embryonic lineages, and explore the complex events involved in the convergence of visceral and primitive streak-derived endoderm. Furthermore, we use single-cell profiling to show that Tal1−/− chimeric embryos display defects in early mesoderm diversification, and we thus demonstrate how combining temporal and transcriptional information can illuminate gene function. Together, this comprehensive delineation of mammalian cell differentiation trajectories in vivo represents a baseline for understanding the effects of gene mutations during development, as well as a roadmap for the optimization of in vitro differentiation protocols for regenerative medicine.

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Species: mouse
Number of cells: 12569
Study size: 690MB

Cell development 
embryo 
Wild-type chimaeras 

A single-cell molecular map of mouse gastrulation and early organogenesis (Wild-type chimaeras)

Blanca Pijuan-Sala, Jonathan A. Griffiths, Carolina Guibentif, Tom W. Hiscock, Wajid Jawaid, Fernando J. Calero-Nieto, Carla Mulas, Ximena Ibarra-Soria, Richard C. V. Tyser, Debbie Lee Lian Ho, Wolf Reik, Shankar Srinivas, Benjamin D. Simons, Jennifer Nichols, John C. Marioni, Berthold Gottgens

Across the animal kingdom, gastrulation represents a key developmental event during which embryonic pluripotent cells diversify into lineage-specific precursors that will generate the adult organism. Here we report the transcriptional profiles of 116,312 single cells from mouse embryos collected at nine sequential time points ranging from 6.5 to 8.5 days post-fertilization. We construct a molecular map of cellular differentiation from pluripotency towards all major embryonic lineages, and explore the complex events involved in the convergence of visceral and primitive streak-derived endoderm. Furthermore, we use single-cell profiling to show that Tal1−/− chimeric embryos display defects in early mesoderm diversification, and we thus demonstrate how combining temporal and transcriptional information can illuminate gene function. Together, this comprehensive delineation of mammalian cell differentiation trajectories in vivo represents a baseline for understanding the effects of gene mutations during development, as well as a roadmap for the optimization of in vitro differentiation protocols for regenerative medicine.

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Species: mouse
Number of cells: 116312
Study size: 4GB

Cell development 
Atlas 
embryo 

A single-cell molecular map of mouse gastrulation and early organogenesis (Atlas)

Blanca Pijuan-Sala, Jonathan A. Griffiths, Carolina Guibentif, Tom W. Hiscock, Wajid Jawaid, Fernando J. Calero-Nieto, Carla Mulas, Ximena Ibarra-Soria, Richard C. V. Tyser, Debbie Lee Lian Ho, Wolf Reik, Shankar Srinivas, Benjamin D. Simons, Jennifer Nichols, John C. Marioni, Berthold Gottgens

Across the animal kingdom, gastrulation represents a key developmental event during which embryonic pluripotent cells diversify into lineage-specific precursors that will generate the adult organism. Here we report the transcriptional profiles of 116,312 single cells from mouse embryos collected at nine sequential time points ranging from 6.5 to 8.5 days post-fertilization. We construct a molecular map of cellular differentiation from pluripotency towards all major embryonic lineages, and explore the complex events involved in the convergence of visceral and primitive streak-derived endoderm. Furthermore, we use single-cell profiling to show that Tal1−/− chimeric embryos display defects in early mesoderm diversification, and we thus demonstrate how combining temporal and transcriptional information can illuminate gene function. Together, this comprehensive delineation of mammalian cell differentiation trajectories in vivo represents a baseline for understanding the effects of gene mutations during development, as well as a roadmap for the optimization of in vitro differentiation protocols for regenerative medicine.

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