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

Stainier, Didier Y R / Bakkers, Jeroen

2023 Volume 16, Issue 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 term(s)	Animals ; Zebrafish ; Lifting ; Heart
Language	English
Publishing date	2023-03-28
Publishing country	England
Document type	Interview
ZDB-ID	2451104-3
ISSN	1754-8411 ; 1754-8403
ISSN (online)	1754-8411
ISSN	1754-8403
DOI	10.1242/dmm.050147
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Article ; Online: Lifting the cloche

Didier Y. R. Stainier / Jeroen Bakkers

Disease Models & Mechanisms, Vol 16, Iss

Jeroen Bakkers interviews Didier Stainier

2023 Volume 5

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.
Keywords	Medicine ; R ; Pathology ; RB1-214
Language	English
Publishing date	2023-05-01T00:00:00Z
Publisher	The Company of Biologists
Document type	Article ; Online
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Article ; Online: Genotype-Phenotype Relationships in the Context of Transcriptional Adaptation and Genetic Robustness.

Jakutis, Gabrielius / Stainier, Didier Y R

Annual review of genetics

2021 Volume 55, Page(s) 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 term(s)	CRISPR-Cas Systems/genetics ; Gene Editing ; Genome ; Genotype ; Phenotype
Language	English
Publishing date	2021-07-27
Publishing country	United States
Document type	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
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Article: Genetics in Light of Transcriptional Adaptation.

Kontarakis, Zacharias / Stainier, Didier Y R

Trends in genetics : TIG

2020 Volume 36, Issue 12, Page(s) 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 term(s)	Adaptation, Physiological ; Animals ; Gene Expression Regulation ; Models, Biological ; Plants ; RNA Stability ; RNA, Messenger/chemistry ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Transcription, Genetic
Chemical Substances	RNA, Messenger
Language	English
Publishing date	2020-09-11
Publishing country	England
Document type	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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Article ; 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 Volume 121, Issue 3, Page(s) 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 term(s)	Animals ; Zebrafish/genetics ; Degrons ; Perciformes ; Myocytes, Cardiac ; Alleles
Language	English
Publishing date	2024-01-09
Publishing country	United States
Document type	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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Article ; Online: Sculpting the heart: Cellular mechanisms shaping valves and trabeculae.

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

Current opinion in cell biology

2021 Volume 73, Page(s) 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 term(s)	Cell Movement ; Heart Valves ; Morphogenesis ; Myocytes, Cardiac ; Organogenesis
Language	English
Publishing date	2021-06-17
Publishing country	England
Document type	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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Article ; 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 Volume 19, Issue 6, Page(s) 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 term(s)	Animals ; Caenorhabditis elegans/genetics ; Acclimatization ; RNA ; RNA, Messenger/genetics ; Nucleotides
Chemical Substances	RNA (63231-63-0) ; RNA, Messenger ; Nucleotides
Language	English
Publishing date	2023-06-29
Publishing country	United States
Document type	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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Article: 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
Language	English
Publishing date	2024-03-13
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.12.584570
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Article ; 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 Volume 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 term(s)	Animals ; Apelin/metabolism ; Endocardium/metabolism ; Myocytes, Cardiac/metabolism ; Neuregulins/metabolism ; Zebrafish/metabolism ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
Chemical Substances	Apelin ; Neuregulins ; Zebrafish Proteins
Language	English
Publishing date	2022-02-28
Publishing country	England
Document type	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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Article ; Online: Transcriptional adaptation: a mechanism underlying genetic robustness.

Sztal, Tamar E / Stainier, Didier Y R

Development (Cambridge, England)

2020 Volume 147, Issue 15

Abstract: Mutations play a crucial role in evolution as they provide the genetic variation that allows evolutionary change. Although some mutations in regulatory elements or coding regions can be beneficial, a large number of them disrupt gene function and reduce ... ...

Abstract	Mutations play a crucial role in evolution as they provide the genetic variation that allows evolutionary change. Although some mutations in regulatory elements or coding regions can be beneficial, a large number of them disrupt gene function and reduce fitness. Organisms utilize several mechanisms to compensate for the damaging consequences of genetic perturbations. One such mechanism is the recently identified process of transcriptional adaptation (TA): during this event, mutations that cause mutant mRNA degradation trigger the transcriptional modulation of so-called adapting genes. In some cases, for example when one (or more) of the upregulated genes is functionally redundant with the mutated gene, this process compensates for the loss of the mutated gene's product. Notably, unlike other mechanisms underlying genetic robustness, TA is not triggered by the loss of protein function, an observation that has prompted studies into the machinery of TA and the contexts in which it functions. Here, we review the discovery and current understanding of TA, and discuss how its main features appear to be conserved across species. In light of these findings, we also speculate on the importance of TA in the context of human disease, and provide some recommendations for genome-editing strategies that should be more effective.
MeSH term(s)	Adaptation, Physiological ; Animals ; Humans ; RNA Stability ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Transcription, Genetic
Chemical Substances	RNA, Messenger
Language	English
Publishing date	2020-08-14
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.186452
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