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  1. Article ; Online: Mutation of p53 increases the competitive ability of pluripotent stem cells.

    Perez Montero, Salvador / Paul, Pranab K / di Gregorio, Aida / Bowling, Sarah / Shepherd, Solomon / Fernandes, Nadia J / Lima, Ana / Pérez-Carrasco, Rubén / Rodriguez, Tristan A

    Development (Cambridge, England)

    2024  Volume 151, Issue 2

    Abstract: During development, the rate of tissue growth is determined by the relative balance of cell division and cell death. Cell competition is a fitness quality-control mechanism that contributes to this balance by eliminating viable cells that are less fit ... ...

    Abstract During development, the rate of tissue growth is determined by the relative balance of cell division and cell death. Cell competition is a fitness quality-control mechanism that contributes to this balance by eliminating viable cells that are less fit than their neighbours. The mutations that confer cells with a competitive advantage and the dynamics of the interactions between winner and loser cells are not well understood. Here, we show that embryonic cells lacking the tumour suppressor p53 are 'super-competitors' that eliminate their wild-type neighbours through the direct induction of apoptosis. This elimination is context dependent, as it does not occur when cells are pluripotent and it is triggered by the onset of differentiation. Furthermore, by combining mathematical modelling and cell-based assays we show that the elimination of wild-type cells is not through competition for space or nutrients, but instead is mediated by short-range interactions that are dependent on the local cell neighbourhood. This highlights the importance of the local cell neighbourhood and the competitive interactions within this neighbourhood for the regulation of proliferation during early embryonic development.
    MeSH term(s) Cell Communication/physiology ; Tumor Suppressor Protein p53/genetics ; Mutation/genetics ; Apoptosis/genetics ; Pluripotent Stem Cells
    Chemical Substances Tumor Suppressor Protein p53
    Language English
    Publishing date 2024-01-19
    Publishing country England
    Document type Journal Article
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.202503
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Cell competition: the winners and losers of fitness selection.

    Bowling, Sarah / Lawlor, Katerina / Rodríguez, Tristan A

    Development (Cambridge, England)

    2019  Volume 146, Issue 13

    Abstract: The process of cell competition results in the 'elimination of cells that are viable but less fit than surrounding cells'. Given the highly heterogeneous nature of our tissues, it seems increasingly likely that cells are engaged in a 'survival of the ... ...

    Abstract The process of cell competition results in the 'elimination of cells that are viable but less fit than surrounding cells'. Given the highly heterogeneous nature of our tissues, it seems increasingly likely that cells are engaged in a 'survival of the fittest' battle throughout life. The process has a myriad of positive roles in the organism: it selects against mutant cells in developing tissues, prevents the propagation of oncogenic cells and eliminates damaged cells during ageing. However, 'super-fit' cancer cells can exploit cell competition mechanisms to expand and spread. Here, we review the regulation, roles and risks of cell competition in organism development, ageing and disease.
    MeSH term(s) Aging/physiology ; Animals ; Cell Communication/physiology ; Cell Physiological Phenomena/genetics ; Cellular Microenvironment/physiology ; Competitive Behavior/physiology ; Genetic Fitness/physiology ; Humans ; Reproduction/physiology ; Selection, Genetic/physiology
    Language English
    Publishing date 2019-07-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.167486
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Book ; Online: How to Keep Your faith in an Upside Down World

    Bowling, Sarah

    2011  

    Abstract: We live in a crazy and upside down world. Bad is good, sick is excellent, the bomb is something terrific and the list goes on. Sarah Bowling knows what it means to have a cause and be concerned, confronted, compelled, corrupted, and consumed by it! ... ...

    Abstract We live in a crazy and upside down world. Bad is good, sick is excellent, the bomb is something terrific and the list goes on. Sarah Bowling knows what it means to have a cause and be concerned, confronted, compelled, corrupted, and consumed by it! Shortly before she was married, Sarah had a confrontation with God. Not only did it turn her world upside down, but it had a radical ripple effect on everyone she encountered from that day forward. In Upside Down, Sarah gives readers the fire and passion to seek their own life-changing encounter with the living God and the will to live in a
    Language English
    Size Online-Ressource (145 p.)
    Publisher Destiny Image, Inc
    Publishing place Shippensburg
    Document type Book ; Online
    Note Description based upon print version of record
    ISBN 9780768426632 ; 0768426634
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  4. Article ; Online: A mouse model with high clonal barcode diversity for joint lineage, transcriptomic, and epigenomic profiling in single cells.

    Li, Li / Bowling, Sarah / McGeary, Sean E / Yu, Qi / Lemke, Bianca / Alcedo, Karel / Jia, Yuemeng / Liu, Xugeng / Ferreira, Mark / Klein, Allon M / Wang, Shou-Wen / Camargo, Fernando D

    Cell

    2023  Volume 186, Issue 23, Page(s) 5183–5199.e22

    Abstract: Cellular lineage histories and their molecular states encode fundamental principles of tissue development and homeostasis. Current lineage-recording mouse models have insufficient barcode diversity and single-cell lineage coverage for profiling tissues ... ...

    Abstract Cellular lineage histories and their molecular states encode fundamental principles of tissue development and homeostasis. Current lineage-recording mouse models have insufficient barcode diversity and single-cell lineage coverage for profiling tissues composed of millions of cells. Here, we developed DARLIN, an inducible Cas9 barcoding mouse line that utilizes terminal deoxynucleotidyl transferase (TdT) and 30 CRISPR target sites. DARLIN is inducible, generates massive lineage barcodes across tissues, and enables the detection of edited barcodes in ∼70% of profiled single cells. Using DARLIN, we examined fate bias within developing hematopoietic stem cells (HSCs) and revealed unique features of HSC migration. Additionally, we established a protocol for joint transcriptomic and epigenomic single-cell measurements with DARLIN and found that cellular clonal memory is associated with genome-wide DNA methylation rather than gene expression or chromatin accessibility. DARLIN will enable the high-resolution study of lineage relationships and their molecular signatures in diverse tissues and physiological contexts.
    MeSH term(s) Animals ; Mice ; Transcriptome/genetics ; Epigenomics ; Cell Lineage/genetics ; Gene Expression Profiling ; Disease Models, Animal ; DNA
    Chemical Substances DNA (9007-49-2)
    Language English
    Publishing date 2023-10-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2023.09.019
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  5. Article ; Online: Cell Competition and Its Role in the Regulation of Cell Fitness from Development to Cancer.

    Di Gregorio, Aida / Bowling, Sarah / Rodriguez, Tristan Argeo

    Developmental cell

    2016  Volume 38, Issue 6, Page(s) 621–634

    Abstract: Cell competition is a cell fitness-sensing mechanism conserved from insects to mammals that eliminates those cells that, although viable, are less fit than their neighbors. An important implication of cell competition is that cellular fitness is not only ...

    Abstract Cell competition is a cell fitness-sensing mechanism conserved from insects to mammals that eliminates those cells that, although viable, are less fit than their neighbors. An important implication of cell competition is that cellular fitness is not only a cell-intrinsic property but is also determined relative to the fitness of neighboring cells: a cell that is of suboptimal fitness in one context may be "super-fit" in the context of a different cell population. Here we discuss the mechanisms by which cell competition measures and communicates cell fitness levels and the implications of this mechanism for development, regeneration, and tumor progression.
    MeSH term(s) Animals ; Cell Communication/genetics ; Drosophila melanogaster/cytology ; Drosophila melanogaster/genetics ; Drosophila melanogaster/growth & development ; Embryonic Development/genetics ; Genetic Fitness ; Humans ; Neoplasms/genetics
    Language English
    Publishing date 2016-09-19
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2016.08.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Lifelong multilineage contribution by embryonic-born blood progenitors.

    Patel, Sachin H / Christodoulou, Constantina / Weinreb, Caleb / Yu, Qi / da Rocha, Edroaldo Lummertz / Pepe-Mooney, Brian J / Bowling, Sarah / Li, Li / Osorio, Fernando G / Daley, George Q / Camargo, Fernando D

    Nature

    2022  Volume 606, Issue 7915, Page(s) 747–753

    Abstract: Haematopoietic stem cells (HSCs) arise in the embryo from the arterial endothelium through a process known as the endothelial-to-haematopoietic transition (EHT) ...

    Abstract Haematopoietic stem cells (HSCs) arise in the embryo from the arterial endothelium through a process known as the endothelial-to-haematopoietic transition (EHT)
    MeSH term(s) Aging ; Animals ; Cell Lineage ; Embryo, Mammalian/cytology ; Hematopoiesis ; Hematopoietic Stem Cells/cytology ; Mice ; Multipotent Stem Cells/cytology
    Language English
    Publishing date 2022-06-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-022-04804-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: DRP1 levels determine the apoptotic threshold during embryonic differentiation through a mitophagy-dependent mechanism.

    Pernaute, Barbara / Pérez-Montero, Salvador / Sánchez Nieto, Juan Miguel / Di Gregorio, Aida / Lima, Ana / Lawlor, Katerina / Bowling, Sarah / Liccardi, Gianmaria / Tomás, Alejandra / Meier, Pascal / Sesaki, Hiromi / Rutter, Guy A / Barbaric, Ivana / Rodríguez, Tristan A

    Developmental cell

    2022  Volume 57, Issue 11, Page(s) 1316–1330.e7

    Abstract: The changes that drive differentiation facilitate the emergence of abnormal cells that need to be removed before they contribute to further development or the germline. Consequently, in mice in the lead-up to gastrulation, ∼35% of embryonic cells are ... ...

    Abstract The changes that drive differentiation facilitate the emergence of abnormal cells that need to be removed before they contribute to further development or the germline. Consequently, in mice in the lead-up to gastrulation, ∼35% of embryonic cells are eliminated. This elimination is caused by hypersensitivity to apoptosis, but how it is regulated is poorly understood. Here, we show that upon exit of naive pluripotency, mouse embryonic stem cells lower their mitochondrial apoptotic threshold, and this increases their sensitivity to cell death. We demonstrate that this enhanced apoptotic response is induced by a decrease in mitochondrial fission due to a reduction in the activity of dynamin-related protein 1 (DRP1). Furthermore, we show that in naive pluripotent cells, DRP1 prevents apoptosis by promoting mitophagy. In contrast, during differentiation, reduced mitophagy levels facilitate apoptosis. Together, these results indicate that during early mammalian development, DRP1 regulation of mitophagy determines the apoptotic response.
    MeSH term(s) Animals ; Apoptosis/physiology ; Dynamins/metabolism ; Mammals/metabolism ; Mice ; Mitochondria/metabolism ; Mitochondrial Dynamics/physiology ; Mitophagy/physiology
    Chemical Substances Dnm1l protein, mouse (EC 3.6.5.5) ; Dynamins (EC 3.6.5.5)
    Language English
    Publishing date 2022-05-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2022.04.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Genetic Deletion of Hesx1 Promotes Exit from the Pluripotent State and Impairs Developmental Diapause.

    Pozzi, Sara / Bowling, Sarah / Apps, John / Brickman, Joshua M / Rodriguez, Tristan A / Martinez-Barbera, Juan Pedro

    Stem cell reports

    2019  Volume 13, Issue 6, Page(s) 970–979

    Abstract: The role of the homeobox transcriptional repressor HESX1 in embryonic stem cells (ESCs) remains mostly unknown. Here, we show that Hesx1 is expressed in the preimplantation mouse embryo, where it is required during developmental diapause. Absence of ... ...

    Abstract The role of the homeobox transcriptional repressor HESX1 in embryonic stem cells (ESCs) remains mostly unknown. Here, we show that Hesx1 is expressed in the preimplantation mouse embryo, where it is required during developmental diapause. Absence of Hesx1 leads to reduced expression of epiblast and primitive endoderm determinants and failure of diapaused embryos to resume embryonic development after implantation. Genetic deletion of Hesx1 impairs self-renewal and promotes differentiation toward epiblast by reducing the expression of pluripotency factors and decreasing the activity of LIF/STAT3 signaling. We reveal that Hesx1-deficient ESCs show elevated ERK pathway activation, resulting in accelerated differentiation toward primitive endoderm, which can be prevented by overexpression of Hesx1. Together, our data provide evidence for a novel role of Hesx1 in the control of self-renewal and maintenance of the undifferentiated state in ESCs and mouse embryos.
    MeSH term(s) Animals ; Biomarkers ; Cell Differentiation/genetics ; Cell Self Renewal/genetics ; Diapause/genetics ; Embryonic Development ; Embryonic Stem Cells/cytology ; Embryonic Stem Cells/metabolism ; Fluorescent Antibody Technique ; Gene Deletion ; Gene Expression Regulation ; Homeodomain Proteins ; Leukemia Inhibitory Factor/metabolism ; MAP Kinase Signaling System ; Mice ; Models, Biological ; Phenotype ; Pluripotent Stem Cells/cytology ; Pluripotent Stem Cells/metabolism ; Repressor Proteins/deficiency ; Signal Transduction
    Chemical Substances Biomarkers ; Hesx1 protein, mouse ; Homeodomain Proteins ; Leukemia Inhibitory Factor ; Lif protein, mouse ; Repressor Proteins
    Language English
    Publishing date 2019-11-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2720528-9
    ISSN 2213-6711 ; 2213-6711
    ISSN (online) 2213-6711
    ISSN 2213-6711
    DOI 10.1016/j.stemcr.2019.10.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: An Engineered CRISPR-Cas9 Mouse Line for Simultaneous Readout of Lineage Histories and Gene Expression Profiles in Single Cells.

    Bowling, Sarah / Sritharan, Duluxan / Osorio, Fernando G / Nguyen, Maximilian / Cheung, Priscilla / Rodriguez-Fraticelli, Alejo / Patel, Sachin / Yuan, Wei-Chien / Fujiwara, Yuko / Li, Bin E / Orkin, Stuart H / Hormoz, Sahand / Camargo, Fernando D

    Cell

    2020  Volume 181, Issue 7, Page(s) 1693–1694

    Language English
    Publishing date 2020-06-24
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2020.06.018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: An Engineered CRISPR-Cas9 Mouse Line for Simultaneous Readout of Lineage Histories and Gene Expression Profiles in Single Cells.

    Bowling, Sarah / Sritharan, Duluxan / Osorio, Fernando G / Nguyen, Maximilian / Cheung, Priscilla / Rodriguez-Fraticelli, Alejo / Patel, Sachin / Yuan, Wei-Chien / Fujiwara, Yuko / Li, Bin E / Orkin, Stuart H / Hormoz, Sahand / Camargo, Fernando D

    Cell

    2020  Volume 181, Issue 6, Page(s) 1410–1422.e27

    Abstract: Tracing the lineage history of cells is key to answering diverse and fundamental questions in biology. Coupling of cell ancestry information with other molecular readouts represents an important goal in the field. Here, we describe the CRISPR array ... ...

    Abstract Tracing the lineage history of cells is key to answering diverse and fundamental questions in biology. Coupling of cell ancestry information with other molecular readouts represents an important goal in the field. Here, we describe the CRISPR array repair lineage tracing (CARLIN) mouse line and corresponding analysis tools that can be used to simultaneously interrogate the lineage and transcriptomic information of single cells in vivo. This model exploits CRISPR technology to generate up to 44,000 transcribed barcodes in an inducible fashion at any point during development or adulthood, is compatible with sequential barcoding, and is fully genetically defined. We have used CARLIN to identify intrinsic biases in the activity of fetal liver hematopoietic stem cell (HSC) clones and to uncover a previously unappreciated clonal bottleneck in the response of HSCs to injury. CARLIN also allows the unbiased identification of transcriptional signatures associated with HSC activity without cell sorting.
    MeSH term(s) Animals ; CRISPR-Cas Systems/genetics ; Cell Line ; Cell Lineage/genetics ; Clustered Regularly Interspaced Short Palindromic Repeats/genetics ; Female ; Flow Cytometry/methods ; Hematopoietic Stem Cells/physiology ; Male ; Mice ; Transcriptome/genetics ; Transduction, Genetic/methods
    Language English
    Publishing date 2020-05-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2020.04.048
    Database MEDical Literature Analysis and Retrieval System OnLINE

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