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  1. Artikel ; Online: Lifting the cloche: Jeroen Bakkers interviews Didier Stainier.

    Stainier, Didier Y R / Bakkers, Jeroen

    Disease models & mechanisms

    2023  Band 16, Heft 5

    Abstract: Didier Stainier is Director of the Department of Developmental Genetics at the Max Planck Institute ... organism to investigate cardiac development, disease and regeneration. Jeroen and Didier met up at a recent ... name and Didier's commitment to mentorship. ...

    Abstract Didier Stainier is Director of the Department of Developmental Genetics at the Max Planck Institute for Heart and Lung Research in Bad Nauheim, Germany. He became acquainted with the zebrafish model as a PhD student in Walter Gilbert's lab at Harvard, which motivated him to champion the use of this powerful model organism to study heart development as a postdoctoral fellow with Mark Fishman at Massachusetts General Hospital. Although his scientific focus has expanded significantly since then, zebrafish modelling and heart development and regeneration remain key topics in his research. The developmental biology and zebrafish modelling communities have embraced him as an inspiring mentor and advocate for basic research. Jeroen Bakkers is a group leader at the Hubrecht Institute for Developmental Biology and Stem Cell Research and Professor of Molecular Cardiogenetics at the University Medical Center Utrecht, The Netherlands. Jeroen did hid PhD with Herman Spaink at Leiden University, The Netherlands. A short visit to Massachusetts Institute of Technology during his doctoral training introduced him to the zebrafish model, which he applied to his PhD project. Zebrafish development remained the focus of his career, including during his postdoctoral training in the lab of Matthias Hammerschmidt at the Max Planck Institute of Immunology and Epigenetics in Freiburg and in his own lab at the Hubrecht Institute, where his group uses this powerful model organism to investigate cardiac development, disease and regeneration. Jeroen and Didier met up at a recent conference to talk about their shared interest in cardiac regeneration, a zebrafish mutant with a curious name and Didier's commitment to mentorship.
    Mesh-Begriff(e) Animals ; Zebrafish ; Lifting ; Heart
    Sprache Englisch
    Erscheinungsdatum 2023-03-28
    Erscheinungsland England
    Dokumenttyp Interview
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.050147
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: A β-catenin chromobody-based probe highlights endothelial maturation during vascular morphogenesis in vivo.

    Gauvrit, Sébastien / Zhao, Shengnan / Rothbauer, Ulrich / Stainier, Didier Y R

    Development (Cambridge, England)

    2024  Band 151, Heft 11

    Abstract: Visualization of protein dynamics is a crucial step in understanding cellular processes. Chromobodies, fluorescently labelled single-domain antibodies, have emerged as versatile probes for live cell imaging of endogenous proteins. However, how these ... ...

    Abstract Visualization of protein dynamics is a crucial step in understanding cellular processes. Chromobodies, fluorescently labelled single-domain antibodies, have emerged as versatile probes for live cell imaging of endogenous proteins. However, how these chromobodies behave in vivo and how accurately they monitor tissue changes remain poorly explored. Here, we generated an endothelial-specific β-catenin chromobody-derived probe and analyzed its expression pattern during cardiovascular development in zebrafish. Using high-resolution confocal imaging, we show that the chromobody signal correlates with the localization of β-catenin in the nucleus and at cell-cell junctions, and thereby can be used to assess endothelial maturation. Loss of Cadherin 5 strongly affects the localization of the chromobody at the cell membrane, confirming the cadherin-based adherens junction role of β-catenin. Furthermore, using a genetic model to block blood flow, we observed that cell junctions are compromised in most endothelial cells but not in the endocardium, highlighting the heterogeneous response of the endothelium to the lack of blood flow. Overall, our data further expand the use of chromobodies for in vivo applications and illustrate their potential to monitor tissue morphogenesis at high resolution.
    Mesh-Begriff(e) Animals ; Zebrafish/embryology ; Zebrafish/metabolism ; beta Catenin/metabolism ; Cadherins/metabolism ; Cadherins/genetics ; Morphogenesis ; Zebrafish Proteins/metabolism ; Zebrafish Proteins/genetics ; Adherens Junctions/metabolism ; Endothelial Cells/metabolism ; Endothelial Cells/cytology ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/cytology ; Antigens, CD
    Chemische Substanzen beta Catenin ; Cadherins ; Zebrafish Proteins ; cadherin 5 ; Antigens, CD
    Sprache Englisch
    Erscheinungsdatum 2024-06-07
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.202122
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Lifting the cloche

    Didier Y. R. Stainier / Jeroen Bakkers

    Disease Models & Mechanisms, Vol 16, Iss

    Jeroen Bakkers interviews Didier Stainier

    2023  Band 5

    Abstract: Didier Stainier is Director of the Department of Developmental Genetics at the Max Planck Institute ... organism to investigate cardiac development, disease and regeneration. Jeroen and Didier met up at a recent ... name and Didier's commitment to mentorship. ...

    Abstract Didier Stainier is Director of the Department of Developmental Genetics at the Max Planck Institute for Heart and Lung Research in Bad Nauheim, Germany. He became acquainted with the zebrafish model as a PhD student in Walter Gilbert's lab at Harvard, which motivated him to champion the use of this powerful model organism to study heart development as a postdoctoral fellow with Mark Fishman at Massachusetts General Hospital. Although his scientific focus has expanded significantly since then, zebrafish modelling and heart development and regeneration remain key topics in his research. The developmental biology and zebrafish modelling communities have embraced him as an inspiring mentor and advocate for basic research. Jeroen Bakkers is a group leader at the Hubrecht Institute for Developmental Biology and Stem Cell Research and Professor of Molecular Cardiogenetics at the University Medical Center Utrecht, The Netherlands. Jeroen did hid PhD with Herman Spaink at Leiden University, The Netherlands. A short visit to Massachusetts Institute of Technology during his doctoral training introduced him to the zebrafish model, which he applied to his PhD project. Zebrafish development remained the focus of his career, including during his postdoctoral training in the lab of Matthias Hammerschmidt at the Max Planck Institute of Immunology and Epigenetics in Freiburg and in his own lab at the Hubrecht Institute, where his group uses this powerful model organism to investigate cardiac development, disease and regeneration. Jeroen and Didier met up at a recent conference to talk about their shared interest in cardiac regeneration, a zebrafish mutant with a curious name and Didier's commitment to mentorship.
    Schlagwörter Medicine ; R ; Pathology ; RB1-214
    Sprache Englisch
    Erscheinungsdatum 2023-05-01T00:00:00Z
    Verlag The Company of Biologists
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Genotype-Phenotype Relationships in the Context of Transcriptional Adaptation and Genetic Robustness.

    Jakutis, Gabrielius / Stainier, Didier Y R

    Annual review of genetics

    2021  Band 55, Seite(n) 71–91

    Abstract: Genetic manipulations with a robust and predictable outcome are critical to investigate gene function, as well as for therapeutic genome engineering. For many years, knockdown approaches and reagents including RNA interference and antisense ... ...

    Abstract Genetic manipulations with a robust and predictable outcome are critical to investigate gene function, as well as for therapeutic genome engineering. For many years, knockdown approaches and reagents including RNA interference and antisense oligonucleotides dominated functional studies; however, with the advent of precise genome editing technologies, CRISPR-based knockout systems have become the state-of-the-art tools for such studies. These technologies have helped decipher the role of thousands of genes in development and disease. Their use has also revealed how limited our understanding of genotype-phenotype relationships is. The recent discovery that certain mutations can trigger the transcriptional modulation of other genes, a phenomenon called transcriptional adaptation, has provided an additional explanation for the contradicting phenotypes observed in knockdown versus knockout models and increased awareness about the use of each of these approaches. In this review, we first cover the strengths and limitations of different gene perturbation strategies. Then we highlight the diverse ways in which the genotype-phenotype relationship can be discordant between these different strategies. Finally, we review the genetic robustness mechanisms that can lead to such discrepancies, paying special attention to the recently discovered phenomenon of transcriptional adaptation.
    Mesh-Begriff(e) CRISPR-Cas Systems/genetics ; Gene Editing ; Genome ; Genotype ; Phenotype
    Sprache Englisch
    Erscheinungsdatum 2021-07-27
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 207928-8
    ISSN 1545-2948 ; 0066-4170 ; 0066-4197
    ISSN (online) 1545-2948
    ISSN 0066-4170 ; 0066-4197
    DOI 10.1146/annurev-genet-071719-020342
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: Genetics in Light of Transcriptional Adaptation.

    Kontarakis, Zacharias / Stainier, Didier Y R

    Trends in genetics : TIG

    2020  Band 36, Heft 12, Seite(n) 926–935

    Abstract: Genetics has recently benefited from the genome engineering revolution: genes can be knocked out, knocked down, or activated more easily than ever before. This range of genetic manipulations has also provided a range of outcomes, sometimes contradictory. ...

    Abstract Genetics has recently benefited from the genome engineering revolution: genes can be knocked out, knocked down, or activated more easily than ever before. This range of genetic manipulations has also provided a range of outcomes, sometimes contradictory. But how much interesting biology hides within these discrepancies? Recent studies have shown that genetic compensation can be activated by some gene perturbations and not others, hinting that this phenomenon might skew our understanding of the genotype-phenotype relationship. We review the main findings regarding transcriptional adaptation, a newly discovered form of genetic compensation, and discuss their possible implications for establishing and analyzing animal and plant models to study gene function. We also touch upon how this new knowledge could benefit our understanding of disease-causing mutations and help explain cases of low penetrance or variable expressivity in human genetics.
    Mesh-Begriff(e) Adaptation, Physiological ; Animals ; Gene Expression Regulation ; Models, Biological ; Plants ; RNA Stability ; RNA, Messenger/chemistry ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Transcription, Genetic
    Chemische Substanzen RNA, Messenger
    Sprache Englisch
    Erscheinungsdatum 2020-09-11
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 619240-3
    ISSN 1362-4555 ; 0168-9525 ; 0168-9479
    ISSN (online) 1362-4555
    ISSN 0168-9525 ; 0168-9479
    DOI 10.1016/j.tig.2020.08.008
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  6. Artikel ; Online: Control of cardiac contractions using Cre-lox and degron strategies in zebrafish.

    Juan, Thomas / Bellec, Maëlle / Cardoso, Bárbara / Athéa, Héloïse / Fukuda, Nana / Albu, Marga / Günther, Stefan / Looso, Mario / Stainier, Didier Y R

    Proceedings of the National Academy of Sciences of the United States of America

    2024  Band 121, Heft 3, Seite(n) e2309842121

    Abstract: Cardiac contractions and hemodynamic forces are essential for organ development and homeostasis. Control over cardiac contractions can be achieved pharmacologically or optogenetically. However, these approaches lack specificity or require direct access ... ...

    Abstract Cardiac contractions and hemodynamic forces are essential for organ development and homeostasis. Control over cardiac contractions can be achieved pharmacologically or optogenetically. However, these approaches lack specificity or require direct access to the heart. Here, we compare two genetic approaches to control cardiac contractions by modulating the levels of the essential sarcomeric protein Tnnt2a in zebrafish. We first recombine a newly generated
    Mesh-Begriff(e) Animals ; Zebrafish/genetics ; Degrons ; Perciformes ; Myocytes, Cardiac ; Alleles
    Sprache Englisch
    Erscheinungsdatum 2024-01-09
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2309842121
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  7. Artikel ; Online: Sculpting the heart: Cellular mechanisms shaping valves and trabeculae.

    Gunawan, Felix / Priya, Rashmi / Stainier, Didier Y R

    Current opinion in cell biology

    2021  Band 73, Seite(n) 26–34

    Abstract: The transformation of the heart from a simple tube to a complex organ requires the orchestration of several morphogenetic processes. Two structures critical for cardiac function, the cardiac valves and the trabecular network, are formed through extensive ...

    Abstract The transformation of the heart from a simple tube to a complex organ requires the orchestration of several morphogenetic processes. Two structures critical for cardiac function, the cardiac valves and the trabecular network, are formed through extensive tissue morphogenesis-endocardial cell migration, deadhesion and differentiation into fibroblast-like cells during valve formation, and cardiomyocyte delamination and apico-basal depolarization during trabeculation. Here, we review current knowledge of how these specialized structures acquire their shape by focusing on the underlying cellular behaviors and molecular mechanisms, highlighting findings from in vivo models and briefly discussing the recent advances in cardiac cell culture and organoids.
    Mesh-Begriff(e) Cell Movement ; Heart Valves ; Morphogenesis ; Myocytes, Cardiac ; Organogenesis
    Sprache Englisch
    Erscheinungsdatum 2021-06-17
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1026381-0
    ISSN 1879-0410 ; 0955-0674
    ISSN (online) 1879-0410
    ISSN 0955-0674
    DOI 10.1016/j.ceb.2021.04.009
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  8. Artikel ; Online: Partial sequence identity in a 25-nucleotide long element is sufficient for transcriptional adaptation in the Caenorhabditis elegans act-5/act-3 model.

    Welker, Jordan M / Serobyan, Vahan / Zaker Esfahani, Elhamalsadat / Stainier, Didier Y R

    PLoS genetics

    2023  Band 19, Heft 6, Seite(n) e1010806

    Abstract: Genetic robustness can be achieved via several mechanisms including transcriptional adaptation (TA), a sequence similarity-driven process whereby mutant mRNA degradation products modulate, directly or indirectly, the expression of so-called adapting ... ...

    Abstract Genetic robustness can be achieved via several mechanisms including transcriptional adaptation (TA), a sequence similarity-driven process whereby mutant mRNA degradation products modulate, directly or indirectly, the expression of so-called adapting genes. To identify the sequences required for this process, we utilized a transgenic approach in Caenorhabditis elegans, combining an overexpression construct for a mutant gene (act-5) and a fluorescent reporter for the corresponding adapting gene (act-3). Analyzing a series of modifications for each construct, we identified, in the 5' regulatory region of the act-3 locus, a 25-base pair (bp) element which exhibits 60% identity with a sequence in the act-5 mRNA and which, in the context of a minimal promoter, is sufficient to induce ectopic expression of the fluorescent reporter. The 25 nucleotide (nt) element in the act-5 mRNA lies between the premature termination codon (PTC) and the next exon/exon junction, suggesting the importance of this region of the mutant mRNA for TA. Additionally, we found that single-stranded RNA injections of this 25 nt element from act-5 into the intestine of wild-type larvae led to higher levels of adapting gene (act-3) mRNA. Different models have been proposed to underlie the modulation of gene expression during TA including chromatin remodeling, the inhibition of antisense RNAs, the release of transcriptional pausing, and the suppression of premature transcription termination, and our data clearly show the importance of the regulatory region of the adapting gene in this particular act-5/act-3 TA model. Our findings also suggest that RNA fragments can modulate the expression of loci exhibiting limited sequence similarity, possibly a critical observation when designing RNA based therapies.
    Mesh-Begriff(e) Animals ; Caenorhabditis elegans/genetics ; Acclimatization ; RNA ; RNA, Messenger/genetics ; Nucleotides
    Chemische Substanzen RNA (63231-63-0) ; RNA, Messenger ; Nucleotides
    Sprache Englisch
    Erscheinungsdatum 2023-06-29
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2186725-2
    ISSN 1553-7404 ; 1553-7390
    ISSN (online) 1553-7404
    ISSN 1553-7390
    DOI 10.1371/journal.pgen.1010806
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  9. Artikel: Border-zone cardiomyocytes and macrophages contribute to remodeling of the extracellular matrix to promote cardiomyocyte invasion during zebrafish cardiac regeneration.

    Constanty, Florian / Wu, Bailin / Wei, Ke-Hsuan / Lin, I-Ting / Dallmann, Julia / Guenther, Stefan / Lautenschlaeger, Till / Priya, Rashmi / Lai, Shih-Lei / Stainier, Didier Y R / Beisaw, Arica

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Despite numerous advances in our understanding of zebrafish cardiac regeneration, an aspect that remains less studied is how regenerating cardiomyocytes invade, and eventually replace, the collagen-containing fibrotic tissue following injury. Here, we ... ...

    Abstract Despite numerous advances in our understanding of zebrafish cardiac regeneration, an aspect that remains less studied is how regenerating cardiomyocytes invade, and eventually replace, the collagen-containing fibrotic tissue following injury. Here, we provide an in-depth analysis of the process of cardiomyocyte invasion using live-imaging and histological approaches. We observed close interactions between protruding cardiomyocytes and macrophages at the wound border zone, and macrophage-deficient
    Sprache Englisch
    Erscheinungsdatum 2024-03-13
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2024.03.12.584570
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  10. Artikel ; Online: Apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish.

    Qi, Jialing / Rittershaus, Annegret / Priya, Rashmi / Mansingh, Shivani / Stainier, Didier Y R / Helker, Christian S M

    eLife

    2022  Band 11

    Abstract: During cardiac development, endocardial cells (EdCs) produce growth factors to promote myocardial morphogenesis and growth. In particular, EdCs produce neuregulin which is required for ventricular cardiomyocytes (CMs) to seed the multicellular ridges ... ...

    Abstract During cardiac development, endocardial cells (EdCs) produce growth factors to promote myocardial morphogenesis and growth. In particular, EdCs produce neuregulin which is required for ventricular cardiomyocytes (CMs) to seed the multicellular ridges known as trabeculae. Defects in neuregulin signaling, or in endocardial sprouting toward CMs, cause hypotrabeculation. However, the mechanisms underlying endocardial sprouting remain largely unknown. Here, we first show by live imaging in zebrafish embryos that EdCs interact with CMs via dynamic membrane protrusions. After touching CMs, these protrusions remain in close contact with their target despite the vigorous cardiac contractions. Loss of the CM-derived peptide Apelin, or of the Apelin receptor, which is expressed in EdCs, leads to reduced endocardial sprouting and hypotrabeculation. Mechanistically, neuregulin signaling requires endocardial protrusions to induce extracellular signal-regulated kinase (Erk) activity in CMs and trigger their delamination. Altogether, these data show that Apelin signaling-dependent endocardial protrusions modulate CM behavior during trabeculation.
    Mesh-Begriff(e) Animals ; Apelin/metabolism ; Endocardium/metabolism ; Myocytes, Cardiac/metabolism ; Neuregulins/metabolism ; Zebrafish/metabolism ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
    Chemische Substanzen Apelin ; Neuregulins ; Zebrafish Proteins
    Sprache Englisch
    Erscheinungsdatum 2022-02-28
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.73231
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