scholarly journals NK4 Antagonizes Tbx1/10 to Promote Cardiac versus Pharyngeal Muscle Fate in the Ascidian Second Heart Field

PLoS Biology ◽  
2013 ◽  
Vol 11 (12) ◽  
pp. e1001725 ◽  
Author(s):  
Wei Wang ◽  
Florian Razy-Krajka ◽  
Eric Siu ◽  
Alexandra Ketcham ◽  
Lionel Christiaen
Keyword(s):  
Pharyngeal Muscle ◽  
Second Heart Field ◽  
Heart Field

scholarly journals An FGF-driven feed-forward circuit patterns the cardiopharyngeal mesoderm in space and time

2017 ◽  
Author(s):  
Florian Razy-Krajka ◽  
Basile Gravez ◽  
Nicole Kaplan ◽  
Claudia Racioppi ◽  
Wei Wang ◽  
...  
Keyword(s):  
Cell Types ◽  
Mapk Signaling ◽  
Full Potential ◽  
Pharyngeal Muscle ◽  
Feed Forward ◽  
Second Heart Field ◽  
Cell Divisions ◽  
Multipotent Progenitors ◽  
Heart Field ◽  
Head Muscles

AbstractIn embryos, multipotent progenitors divide to produce distinct progeny and express their full potential. In vertebrates, multipotent cardiopharyngeal progenitors produce second-heart-field-derived cardiomyocytes, and branchiomeric skeletal head muscles. However, the mechanisms underlying these early fate choices remain largely elusive. The tunicate Ciona emerged as an attractive model to study early cardiopharyngeal development at high resolution: through two asymmetric and oriented divisions, defined cardiopharyngeal progenitors produce distinct first and second heart precursors, and pharyngeal muscle (aka atrial siphon muscle, ASM) precursors. Here, we demonstrate that differential FGF-MAPK signaling distinguishes between heart and ASM precursors. We characterize a feed-forward circuit that promotes the successive activations of essential ASM determinants, Hand-related, Tbx1/10 and Ebf. Finally, we show that coupling FGF-MAPK restriction and cardiopharyngeal network deployment with cell divisions defines the timing of gene expression and permits the emergence of diverse cell types from multipotent progenitors.

scholarly journals An FGF-driven feed-forward circuit patterns the cardiopharyngeal mesoderm in space and time

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Florian Razy-Krajka ◽  
Basile Gravez ◽  
Nicole Kaplan ◽  
Claudia Racioppi ◽  
Wei Wang ◽  
...  
Keyword(s):  
Cell Types ◽  
Mapk Signaling ◽  
Full Potential ◽  
Pharyngeal Muscle ◽  
Feed Forward ◽  
Second Heart Field ◽  
Cell Divisions ◽  
Multipotent Progenitors ◽  
Heart Field ◽  
Head Muscles

In embryos, multipotent progenitors divide to produce distinct progeny and express their full potential. In vertebrates, multipotent cardiopharyngeal progenitors produce second-heart-field-derived cardiomyocytes, and branchiomeric skeletal head muscles. However, the mechanisms underlying these early fate choices remain largely elusive. The tunicate Ciona emerged as an attractive model to study early cardiopharyngeal development at high resolution: through two asymmetric and oriented divisions, defined cardiopharyngeal progenitors produce distinct first and second heart precursors, and pharyngeal muscle (aka atrial siphon muscle, ASM) precursors. Here, we demonstrate that differential FGF-MAPK signaling distinguishes between heart and ASM precursors. We characterize a feed-forward circuit that promotes the successive activations of essential ASM determinants, Hand-related, Tbx1/10 and Ebf. Finally, we show that coupling FGF-MAPK restriction and cardiopharyngeal network deployment with cell divisions defines the timing of gene expression and permits the emergence of diverse cell types from multipotent progenitors.

scholarly journals Lamb1a regulates atrial growth by limiting excessive, contractility-dependent second heart field addition during zebrafish heart development

2021 ◽  
Author(s):  
Christopher J. Derrick ◽  
Eric J. G. Pollitt ◽  
Ashley Sanchez Sevilla Uruchurtu ◽  
Farah Hussein ◽  
Emily S. Noёl
Keyword(s):  
Heart Development ◽  
Cardiac Development ◽  
Basement Membranes ◽  
Atrioventricular Canal ◽  
Cardiac Morphogenesis ◽  
Heart Morphogenesis ◽  
Second Heart Field ◽  
Heart Field ◽  
Heart Size ◽  
Zebrafish Heart

AbstractDuring early vertebrate heart development, the heart transitions from a linear tube to a complex asymmetric structure. This process includes looping of the tube and ballooning of the emerging cardiac chambers, which occur simultaneously with growth of the heart. A key driver of cardiac growth is deployment of cells from the Second Heart Field (SHF) into both poles of the heart, with cardiac morphogenesis and growth intimately linked in heart development. Laminin is a core component of extracellular matrix (ECM) basement membranes, and although mutations in specific laminin subunits are linked with a variety of cardiac abnormalities, including congenital heart disease and dilated cardiomyopathy, no role for laminin has been identified in early vertebrate heart morphogenesis. We identified dynamic, tissue-specific expression of laminin subunit genes in the developing zebrafish heart, supporting a role for laminins in heart morphogenesis.lamb1amutants exhibit cardiomegaly from 2dpf onwards, with subsequent progressive defects in cardiac morphogenesis characterised by a failure of the chambers to compact around the developing atrioventricular canal. We show that loss oflamb1aresults in excess addition of SHF cells to the atrium, revealing that Lamb1a functions to limit heart size during cardiac development by restricting SHF addition to the venous pole.lamb1amutants exhibit hallmarks of altered haemodynamics, and specifically blocking cardiac contractility inlamb1amutants rescues heart size and atrial SHF addition. Furthermore, we identify that FGF and RA signalling, two conserved pathways promoting SHF addition, are regulated by heart contractility and are dysregulated inlamb1amutants, suggesting that laminin mediates interactions between SHF deployment, heart biomechanics, and biochemical signalling during heart development. Together, this describes the first requirement for laminins in early vertebrate heart morphogenesis, reinforcing the importance of specialised ECM composition in cardiac development.

scholarly journals Expression of the BMP Receptor Alk3 in the Second Heart Field Is Essential for Development of the Dorsal Mesenchymal Protrusion and Atrioventricular Septation

2013 ◽  
Vol 112 (11) ◽  
pp. 1420-1432 ◽  
Author(s):  
Laura E. Briggs ◽  
Aimee L. Phelps ◽  
Elizabeth Brown ◽  
Jayant Kakarla ◽  
Robert H. Anderson ◽  
...  
Keyword(s):  
Second Heart Field ◽  
Bmp Receptor ◽  
Heart Field ◽  
Dorsal Mesenchymal Protrusion ◽  
Atrioventricular Septation

scholarly journals Temporally Distinct Six2 -Positive Second Heart Field Progenitors Regulate Mammalian Heart Development and Disease

Cell Reports ◽  
2017 ◽  
Vol 18 (4) ◽  
pp. 1019-1032 ◽  
Author(s):  
Zhengfang Zhou ◽  
Jingying Wang ◽  
Chaoshe Guo ◽  
Weiting Chang ◽  
Jian Zhuang ◽  
...  
Keyword(s):  
Heart Development ◽  
Second Heart Field ◽  
Mammalian Heart ◽  
Heart Field

scholarly journals Loss of Wnt5a disrupts second heart field cell deployment and may contribute to OFT malformations in DiGeorge syndrome

2014 ◽  
Vol 24 (6) ◽  
pp. 1704-1716 ◽  
Author(s):  
Tanvi Sinha ◽  
Ding Li ◽  
Magali Théveniau-Ruissy ◽  
Mary R. Hutson ◽  
Robert G. Kelly ◽  
...  
Keyword(s):  
Digeorge Syndrome ◽  
Second Heart Field ◽  
Heart Field

scholarly journals A Boolean Model of the Cardiac Gene Regulatory Network Determining First and Second Heart Field Identity

PLoS ONE ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. e46798 ◽  
Author(s):  
Franziska Herrmann ◽  
Alexander Groß ◽  
Dao Zhou ◽  
Hans A. Kestler ◽  
Michael Kühl
Keyword(s):  
Gene Regulatory Network ◽  
Regulatory Network ◽  
Boolean Model ◽  
Second Heart Field ◽  
Cardiac Gene ◽  
Heart Field ◽  
Gene Regulatory

Cardiac embryogenesis

ESC CardioMed ◽  
2018 ◽  
pp. 33-36
Author(s):  
Robert G. Kelly
Keyword(s):  
Progenitor Cells ◽  
Progenitor Cell ◽  
Congenital Heart ◽  
Heart Defects ◽  
Embryonic Heart ◽  
Heart Tube ◽  
Second Heart Field ◽  
Heart Field ◽  
Cell Niche ◽  
The Right

The embryonic heart forms in anterior lateral splanchnic mesoderm and is derived from Mesp1-expressing progenitor cells. During embryonic folding, the earliest differentiating progenitor cells form the linear heart tube in the ventral midline. The heart tube extends in length and loops to the right as new myocardium is progressively added at the venous and arterial poles from multipotent second heart field cardiovascular progenitor cells in contiguous pharyngeal mesoderm. While the linear heart tube gives rise to the left ventricle, the right ventricle, outflow tract, and a large part of atrial myocardium are derived from the second heart field. Progressive myocardial differentiation is controlled by intercellular signals within the progenitor cell niche. The embryonic heart is the template for septation and growth of the four-chambered definitive heart and defects in progenitor cell deployment result in a spectrum of common forms of congenital heart defects.

scholarly journals Tbx1 regulates extracellular matrix-cell interactions in the second heart field

2019 ◽  
Vol 28 (14) ◽  
pp. 2295-2308 ◽  
Author(s):  
Daniela Alfano ◽  
Alessandra Altomonte ◽  
Claudio Cortes ◽  
Marchesa Bilio ◽  
Robert G Kelly ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cultured Cells ◽  
Time Window ◽  
Outflow Tract ◽  
Mouse Embryos ◽  
Cell Interactions ◽  
Deletion Syndrome ◽  
Cardiac Progenitors ◽  
Second Heart Field ◽  
Heart Field

Abstract Tbx1, the major candidate gene for DiGeorge or 22q11.2 deletion syndrome, is required for efficient incorporation of cardiac progenitors of the second heart field (SHF) into the heart. However, the mechanisms by which TBX1 regulates this process are still unclear. Here, we have used two independent models, mouse embryos and cultured cells, to define the role of TBX1 in establishing morphological and dynamic characteristics of SHF in the mouse. We found that loss of TBX1 impairs extracellular matrix (ECM)-integrin-focal adhesion (FA) signaling in both models. Mosaic analysis in embryos suggested that this function is non-cell autonomous, and, in cultured cells, loss of TBX1 impairs cell migration and FAs. Additionally, we found that ECM-mediated integrin signaling is disrupted upon loss of TBX1. Finally, we show that interfering with the ECM-integrin-FA axis between E8.5 and E9.5 in mouse embryos, corresponding to the time window within which TBX1 is required in the SHF, causes outflow tract dysmorphogenesis. Our results demonstrate that TBX1 is required to maintain the integrity of ECM-cell interactions in the SHF and that this interaction is critical for cardiac outflow tract development. More broadly, our data identifies a novel TBX1 downstream pathway as an important player in SHF tissue architecture and cardiac morphogenesis.

scholarly journals Hes1 Is Expressed in the Second Heart Field and Is Required for Outflow Tract Development

PLoS ONE ◽  
2009 ◽  
Vol 4 (7) ◽  
pp. e6267 ◽  
Author(s):  
Francesca Rochais ◽  
Mathieu Dandonneau ◽  
Karim Mesbah ◽  
Thérèse Jarry ◽  
Marie-Geneviève Mattei ◽  
...  
Keyword(s):  
Outflow Tract ◽  
Second Heart Field ◽  
Heart Field
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