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  1. Article ; Online: From signalling to form: the coordination of neural tube patterning.

    Frith, Thomas J R / Briscoe, James / Boezio, Giulia L M

    Current topics in developmental biology

    2023  Volume 159, Page(s) 168–231

    Abstract: The development of the vertebrate spinal cord involves the formation of the neural tube and the generation of multiple distinct cell types. The process starts during gastrulation, combining axial elongation with specification of neural cells and the ... ...

    Abstract The development of the vertebrate spinal cord involves the formation of the neural tube and the generation of multiple distinct cell types. The process starts during gastrulation, combining axial elongation with specification of neural cells and the formation of the neuroepithelium. Tissue movements produce the neural tube which is then exposed to signals that provide patterning information to neural progenitors. The intracellular response to these signals, via a gene regulatory network, governs the spatial and temporal differentiation of progenitors into specific cell types, facilitating the assembly of functional neuronal circuits. The interplay between the gene regulatory network, cell movement, and tissue mechanics generates the conserved neural tube pattern observed across species. In this review we offer an overview of the molecular and cellular processes governing the formation and patterning of the neural tube, highlighting how the remarkable complexity and precision of vertebrate nervous system arises. We argue that a multidisciplinary and multiscale understanding of the neural tube development, paired with the study of species-specific strategies, will be crucial to tackle the open questions.
    MeSH term(s) Neural Tube/embryology ; Neural Tube/metabolism ; Neural Tube/cytology ; Animals ; Body Patterning/genetics ; Gene Expression Regulation, Developmental ; Signal Transduction ; Humans ; Gene Regulatory Networks ; Spinal Cord/embryology ; Spinal Cord/cytology ; Spinal Cord/metabolism ; Cell Differentiation ; Cell Movement
    Language English
    Publishing date 2023-12-08
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ISSN 1557-8933 ; 0070-2153
    ISSN (online) 1557-8933
    ISSN 0070-2153
    DOI 10.1016/bs.ctdb.2023.11.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The developing epicardium regulates cardiac chamber morphogenesis by promoting cardiomyocyte growth.

    Boezio, Giulia L M / Zhao, Shengnan / Gollin, Josephine / Priya, Rashmi / Mansingh, Shivani / Guenther, Stefan / Fukuda, Nana / Gunawan, Felix / Stainier, Didier Y R

    Disease models & mechanisms

    2022  Volume 16, Issue 5

    Abstract: The epicardium, the outermost layer of the heart, is an important regulator of cardiac regeneration. However, a detailed understanding of the crosstalk between the epicardium and myocardium during development requires further investigation. Here, we ... ...

    Abstract The epicardium, the outermost layer of the heart, is an important regulator of cardiac regeneration. However, a detailed understanding of the crosstalk between the epicardium and myocardium during development requires further investigation. Here, we generated three models of epicardial impairment in zebrafish by mutating the transcription factor genes tcf21 and wt1a, and ablating tcf21+ epicardial cells. Notably, all three epicardial impairment models exhibited smaller ventricles. We identified the initial cause of this phenotype as defective cardiomyocyte growth, resulting in reduced cell surface and volume. This failure of cardiomyocyte growth was followed by decreased proliferation and increased abluminal extrusion. By temporally manipulating its ablation, we show that the epicardium is required to support cardiomyocyte growth mainly during early cardiac morphogenesis. By transcriptomic profiling of sorted epicardial cells, we identified reduced expression of FGF and VEGF ligand genes in tcf21-/- hearts, and pharmacological inhibition of these signaling pathways in wild type partially recapitulated the ventricular growth defects. Taken together, these data reveal distinct roles of the epicardium during cardiac morphogenesis and signaling pathways underlying epicardial-myocardial crosstalk.
    MeSH term(s) Animals ; Zebrafish/metabolism ; Myocytes, Cardiac/metabolism ; Ligands ; Vascular Endothelial Growth Factor A/metabolism ; Pericardium/metabolism ; Organogenesis/genetics ; Heart/physiology ; Myocardium/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; WT1 Proteins/genetics ; WT1 Proteins/metabolism ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
    Chemical Substances Ligands ; Vascular Endothelial Growth Factor A ; Transcription Factors ; Wt1a protein, zebrafish ; WT1 Proteins ; Zebrafish Proteins
    Language English
    Publishing date 2022-10-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.049571
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Integration of multiple imaging platforms to uncover cardiovascular defects in adult zebrafish.

    Bensimon-Brito, Anabela / Boezio, Giulia L M / Cardeira-da-Silva, João / Wietelmann, Astrid / Ramkumar, Srinath / Lundegaard, Pia R / Helker, Christian S M / Ramadass, Radhan / Piesker, Janett / Nauerth, Arno / Mueller, Clemens / Stainier, Didier Y R

    Cardiovascular research

    2021  Volume 118, Issue 12, Page(s) 2665–2687

    Abstract: Aims: Mammalian models have been instrumental in investigating adult heart function and human disease. However, electrophysiological differences with human hearts and high costs motivate the need for non-mammalian models. The zebrafish is a well- ... ...

    Abstract Aims: Mammalian models have been instrumental in investigating adult heart function and human disease. However, electrophysiological differences with human hearts and high costs motivate the need for non-mammalian models. The zebrafish is a well-established genetic model to study cardiovascular development and function; however, analysis of cardiovascular phenotypes in adult specimens is particularly challenging as they are opaque.
    Methods and results: Here, we optimized and combined multiple imaging techniques including echocardiography, magnetic resonance imaging, and micro-computed tomography to identify and analyse cardiovascular phenotypes in adult zebrafish. Using alk5a/tgfbr1a mutants as a case study, we observed morphological and functional cardiovascular defects that were undetected with conventional approaches. Correlation analysis of multiple parameters revealed an association between haemodynamic defects and structural alterations of the heart, as observed clinically.
    Conclusion: We report a new, comprehensive, and sensitive platform to identify otherwise indiscernible cardiovascular phenotypes in adult zebrafish.
    MeSH term(s) Animals ; Cardiovascular System ; Echocardiography ; Heart ; Humans ; Mammals ; X-Ray Microtomography ; Zebrafish/genetics
    Language English
    Publishing date 2021-10-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvab310
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 565: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Cardiac function modulates endocardial cell dynamics to shape the cardiac outflow tract.

    Sidhwani, Pragya / Leerberg, Dena M / Boezio, Giulia L M / Capasso, Teresa L / Yang, Hongbo / Chi, Neil C / Roman, Beth L / Stainier, Didier Y R / Yelon, Deborah

    Development (Cambridge, England)

    2020  Volume 147, Issue 12

    Abstract: Physical forces are important participants in the cellular dynamics that shape developing organs. During heart formation, for example, contractility and blood flow generate biomechanical cues that influence patterns of cell behavior. Here, we address the ...

    Abstract Physical forces are important participants in the cellular dynamics that shape developing organs. During heart formation, for example, contractility and blood flow generate biomechanical cues that influence patterns of cell behavior. Here, we address the interplay between function and form during the assembly of the cardiac outflow tract (OFT), a crucial connection between the heart and vasculature that develops while circulation is under way. In zebrafish, we find that the OFT expands via accrual of both endocardial and myocardial cells. However, when cardiac function is disrupted, OFT endocardial growth ceases, accompanied by reduced proliferation and reduced addition of cells from adjacent vessels. The flow-responsive TGFβ receptor Acvrl1 is required for addition of endocardial cells, but not for their proliferation, indicating distinct modes of function-dependent regulation for each of these essential cell behaviors. Together, our results indicate that cardiac function modulates OFT morphogenesis by triggering endocardial cell accumulation that induces OFT lumen expansion and shapes OFT dimensions. Moreover, these morphogenetic mechanisms provide new perspectives regarding the potential causes of cardiac birth defects.
    MeSH term(s) Activin Receptors/antagonists & inhibitors ; Activin Receptors/genetics ; Activin Receptors/metabolism ; Animals ; Animals, Genetically Modified/growth & development ; Animals, Genetically Modified/metabolism ; Cell Proliferation ; Embryo, Nonmammalian/cytology ; Embryo, Nonmammalian/metabolism ; Endocardium/cytology ; Endocardium/metabolism ; Heart/anatomy & histology ; Heart/growth & development ; Heart/physiology ; Morpholinos/metabolism ; Troponin T/antagonists & inhibitors ; Troponin T/genetics ; Troponin T/metabolism ; Zebrafish/growth & development ; Zebrafish/metabolism ; Zebrafish Proteins/antagonists & inhibitors ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
    Chemical Substances Morpholinos ; Troponin T ; Zebrafish Proteins ; tnnt2a protein, zebrafish ; Acvrl1 protein, zebrafish (EC 2.7.1.-) ; Activin Receptors (EC 2.7.11.30)
    Language English
    Publishing date 2020-06-17
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.185900
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ub I Zs.183: Show issues Location:
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    Zs.MG 91: Show issues

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  5. Article ; Online: TGF-β Signaling Promotes Tissue Formation during Cardiac Valve Regeneration in Adult Zebrafish.

    Bensimon-Brito, Anabela / Ramkumar, Srinath / Boezio, Giulia L M / Guenther, Stefan / Kuenne, Carsten / Helker, Christian S M / Sánchez-Iranzo, Héctor / Iloska, Dijana / Piesker, Janett / Pullamsetti, Soni / Mercader, Nadia / Beis, Dimitris / Stainier, Didier Y R

    Developmental cell

    2019  Volume 52, Issue 1, Page(s) 9–20.e7

    Abstract: Cardiac valve disease can lead to severe cardiac dysfunction and is thus a frequent cause of morbidity and mortality. Its main treatment is valve replacement, which is currently greatly limited by the poor recellularization and tissue formation potential ...

    Abstract Cardiac valve disease can lead to severe cardiac dysfunction and is thus a frequent cause of morbidity and mortality. Its main treatment is valve replacement, which is currently greatly limited by the poor recellularization and tissue formation potential of the implanted valves. As we still lack suitable animal models to identify modulators of these processes, here we used adult zebrafish and found that, upon valve decellularization, they initiate a rapid regenerative program that leads to the formation of new functional valves. After injury, endothelial and kidney marrow-derived cells undergo cell cycle re-entry and differentiate into new extracellular matrix-secreting valve cells. The TGF-β signaling pathway promotes the regenerative process by enhancing progenitor cell proliferation as well as valve cell differentiation. These findings reveal a key role for TGF-β signaling in cardiac valve regeneration and establish the zebrafish as a model to identify and test factors promoting cardiac valve recellularization and growth.
    MeSH term(s) Animals ; Cell Cycle ; Cell Differentiation ; Endothelium/cytology ; Endothelium/metabolism ; Extracellular Matrix/metabolism ; Heart Valves/cytology ; Heart Valves/metabolism ; Kidney/cytology ; Kidney/metabolism ; Models, Animal ; Regeneration ; Tissue Engineering/methods ; Transforming Growth Factor beta/metabolism ; Zebrafish/growth & development ; Zebrafish/metabolism
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2019-11-27
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2019.10.027
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5742: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 76: Show issues

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  6. Article ; Online: Disruption of the pancreatic vasculature in zebrafish affects islet architecture and function.

    Mullapudi, Sri Teja / Boezio, Giulia L M / Rossi, Andrea / Marass, Michele / Matsuoka, Ryota L / Matsuda, Hiroki / Helker, Christian S M / Yang, Yu Hsuan Carol / Stainier, Didier Y R

    Development (Cambridge, England)

    2019  Volume 146, Issue 21

    Abstract: A dense local vascular network is crucial for pancreatic endocrine cells to sense metabolites and secrete hormones, and understanding the interactions between the vasculature and the islets may allow for therapeutic modulation in disease conditions. ... ...

    Abstract A dense local vascular network is crucial for pancreatic endocrine cells to sense metabolites and secrete hormones, and understanding the interactions between the vasculature and the islets may allow for therapeutic modulation in disease conditions. Using live imaging in two models of vascular disruption in zebrafish, we identified two distinct roles for the pancreatic vasculature. At larval stages, expression of a dominant negative version of Vegfaa (dnVegfaa) in β-cells led to vascular and endocrine cell disruption with a minor impairment in β-cell function. In contrast, expression of a soluble isoform of Vegf receptor 1 (sFlt1) in β-cells blocked the formation of the pancreatic vasculature and drastically stunted glucose response, although islet architecture was not affected. Notably, these effects of dnVegfaa or sFlt1 were not observed in animals lacking
    MeSH term(s) Animals ; Blood Glucose/analysis ; Gene Expression Regulation, Developmental ; Glucose/metabolism ; Glucose Tolerance Test ; Green Fluorescent Proteins/metabolism ; Islets of Langerhans/cytology ; Ligands ; Microscopy, Fluorescence ; Mutation ; Pancreas/blood supply ; Pancreas/embryology ; Transgenes ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factor Receptor-1/metabolism ; Zebrafish ; Zebrafish Proteins/metabolism
    Chemical Substances Blood Glucose ; Ligands ; Vascular Endothelial Growth Factor A ; Vegfaa protein, zebrafish ; Zebrafish Proteins ; Green Fluorescent Proteins (147336-22-9) ; FLT1 protein, zebrafish (EC 2.7.10.1) ; Vascular Endothelial Growth Factor Receptor-1 (EC 2.7.10.1) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2019-11-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.173674
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Genetic compensation triggered by mutant mRNA degradation.

    El-Brolosy, Mohamed A / Kontarakis, Zacharias / Rossi, Andrea / Kuenne, Carsten / Günther, Stefan / Fukuda, Nana / Kikhi, Khrievono / Boezio, Giulia L M / Takacs, Carter M / Lai, Shih-Lei / Fukuda, Ryuichi / Gerri, Claudia / Giraldez, Antonio J / Stainier, Didier Y R

    Nature

    2019  Volume 568, Issue 7751, Page(s) 193–197

    Abstract: Genetic robustness, or the ability of an organism to maintain fitness in the presence of harmful mutations, can be achieved via protein feedback loops. Previous work has suggested that organisms may also respond to mutations by transcriptional adaptation, ...

    Abstract Genetic robustness, or the ability of an organism to maintain fitness in the presence of harmful mutations, can be achieved via protein feedback loops. Previous work has suggested that organisms may also respond to mutations by transcriptional adaptation, a process by which related gene(s) are upregulated independently of protein feedback loops. However, the prevalence of transcriptional adaptation and its underlying molecular mechanisms are unknown. Here, by analysing several models of transcriptional adaptation in zebrafish and mouse, we uncover a requirement for mutant mRNA degradation. Alleles that fail to transcribe the mutated gene do not exhibit transcriptional adaptation, and these alleles give rise to more severe phenotypes than alleles displaying mutant mRNA decay. Transcriptome analysis in alleles displaying mutant mRNA decay reveals the upregulation of a substantial proportion of the genes that exhibit sequence similarity with the mutated gene's mRNA, suggesting a sequence-dependent mechanism. These findings have implications for our understanding of disease-causing mutations, and will help in the design of mutant alleles with minimal transcriptional adaptation-derived compensation.
    MeSH term(s) Adaptation, Physiological/genetics ; Alleles ; Animals ; Epigenesis, Genetic/genetics ; Histones/metabolism ; Mice ; Mutation ; RNA Stability/genetics ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Transcription, Genetic/genetics ; Up-Regulation/genetics ; Zebrafish/genetics
    Chemical Substances Histones ; RNA, Messenger
    Language English
    Publishing date 2019-04-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-019-1064-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 26: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 9: Show issues
    Zs.MO 244: Show issues

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