Fashioning the vertebrate heart: earliest embryonic decisions

Development ◽  
1997 ◽  
Vol 124 (11) ◽  
pp. 2099-2117 ◽  
Author(s):  
M.C. Fishman ◽  
K.R. Chien
Keyword(s):  
Caenorhabditis Elegans ◽  
Progenitor Cells ◽  
Cell Fate ◽  
Cellular Differentiation ◽  
Higher Order ◽  
Pattern Generation ◽  
Heart Tube ◽  
Form And Function ◽  
Heart Field ◽  
And Function

Our goal here is to set out the types of unitary decisions made by heart progenitor cells, from their appearance in the heart field until they form the simple heart tube. This provides a context to evaluate cell fate, lineage and, finally, morphogenetic decisions that configure global heart form and function. Some paradigms for cellular differentiation and for pattern generation may be borrowed from invertebrates, but neither Drosophila nor Caenorhabditis elegans suffice to unravel higher order decisions. Genetic analyses in mouse and zebrafish may provide one entrance to these pathways.

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.

Caenorhabditis elegans operons: form and function

2003 ◽  
Vol 4 (2) ◽  
pp. 110-118 ◽  
Author(s):  
Thomas Blumenthal ◽  
Kathy Seggerson Gleason
Keyword(s):  
Caenorhabditis Elegans ◽  
Form And Function ◽  
And Function

Exploring the Caenorhabditis elegans and Drosophila melanogaster genomes to understand neuropeptide and peptidase function

2000 ◽  
Vol 28 (4) ◽  
pp. 464-469 ◽  
Author(s):  
D. Coates ◽  
R. Siviter ◽  
R. E. Isaac
Keyword(s):  
Drosophila Melanogaster ◽  
Caenorhabditis Elegans ◽  
Comparative Studies ◽  
Gene Families ◽  
Human Condition ◽  
Form And Function ◽  
And Function ◽  
The Human Condition

Comparison of peptidase gene families in the newly released Drosophila melanogaster and Caenorhabditis elegans genomes highlights important differences in peptidase distributions with relevance to the evolution of both form and function in these two organisms and can help to identify the most appropriate model when using comparative studies relevant to the human condition.

scholarly journals Hox-dependent coordination of cardiac progenitor cell patterning and differentiation

2020 ◽  
Author(s):  
Sonia Stefanovic ◽  
Brigitte Laforest ◽  
Jean-Pierre Desvignes ◽  
Fabienne Lescroart ◽  
Laurent Argiro ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Heart Defects ◽  
Embryonic Stem ◽  
Chromatin Accessibility ◽  
Cardiac Differentiation ◽  
Cardiac Progenitor Cells ◽  
Heart Tube ◽  
Atrioventricular Septal Defects ◽  
Genome Wide ◽  
Heart Field

SUMMARYPerturbation of addition of second heart field (SHF) cardiac progenitor cells to the poles of the heart tube results in congenital heart defects (CHD). The transcriptional programs and upstream regulatory events operating in different subpopulations of the SHF remain unclear. Here, we profile the transcriptome and chromatin accessibility of anterior and posterior SHF sub-populations at genome-wide levels and demonstrate that Hoxb1 negatively regulates differentiation in the posterior SHF. Spatial mis-expression of Hoxb1 in the anterior SHF results in hypoplastic right ventricle. Activation of Hoxb1 in embryonic stem cells arrests cardiac differentiation, whereas Hoxb1-deficient embryos display premature cardiac differentiation. Moreover, ectopic differentiation in the posterior SHF of embryos lacking both Hoxb1 and its paralog Hoxa1 results in atrioventricular septal defects. Our results show that Hoxb1 plays a key role in patterning cardiac progenitor cells that contribute to both cardiac poles and provide new insights into the pathogenesis of CHD.

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.

Computational Model for the Transition From Peristaltic to Pulsatile Flow in the Embryonic Heart Tube

2006 ◽  
Vol 129 (3) ◽  
pp. 441-449 ◽  
Author(s):  
Larry A. Taber ◽  
Jinmei Zhang ◽  
Renato Perucchio
Keyword(s):  
Computational Model ◽  
Pulsatile Flow ◽  
Embryonic Heart ◽  
Single Muscle ◽  
Heart Tube ◽  
Endocardial Cushions ◽  
Form And Function ◽  
Flow Parameters ◽  
And Function ◽  
Good Agreement

Early in development, the heart is a single muscle-wrapped tube without formed valves. Yet survival of the embryo depends on the ability of this tube to pump blood at steadily increasing rates and pressures. Developmental biologists historically have speculated that the heart tube pumps via a peristaltic mechanism, with a wave of contraction propagating from the inflow to the outflow end. Physiological measurements, however, have shown that the flow becomes pulsatile in character quite early in development, before the valves form. Here, we use a computational model for flow though the embryonic heart to explore the pumping mechanism. Results from the model show that endocardial cushions, which are valve primordia arising near the ends of the tube, induce a transition from peristaltic to pulsatile flow. Comparison of numerical results with published experimental data shows reasonably good agreement for various pressure and flow parameters. This study illustrates the interrelationship between form and function in the early embryonic heart.

scholarly journals Hox-dependent coordination of mouse cardiac progenitor cell patterning and differentiation

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Sonia Stefanovic ◽  
Brigitte Laforest ◽  
Jean-Pierre Desvignes ◽  
Fabienne Lescroart ◽  
Laurent Argiro ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Heart Defects ◽  
Embryonic Stem ◽  
Chromatin Accessibility ◽  
Cardiac Differentiation ◽  
Cardiac Progenitor Cells ◽  
Heart Tube ◽  
Atrioventricular Septal Defects ◽  
Genome Wide ◽  
Heart Field

Perturbation of addition of second heart field (SHF) cardiac progenitor cells to the poles of the heart tube results in congenital heart defects (CHD). The transcriptional programs and upstream regulatory events operating in different subpopulations of the SHF remain unclear. Here, we profile the transcriptome and chromatin accessibility of anterior and posterior SHF sub-populations at genome-wide levels and demonstrate that Hoxb1 negatively regulates differentiation in the posterior SHF. Spatial mis-expression of Hoxb1 in the anterior SHF results in hypoplastic right ventricle. Activation of Hoxb1 in embryonic stem cells arrests cardiac differentiation, whereas Hoxb1-deficient mouse embryos display premature cardiac differentiation. Moreover, ectopic differentiation in the posterior SHF of embryos lacking both Hoxb1 and its paralog Hoxa1 results in atrioventricular septal defects. Our results show that Hoxb1 plays a key role in patterning cardiac progenitor cells that contribute to both cardiac poles and provide new insights into the pathogenesis of CHD.

scholarly journals Epigenetics in Insects: Genome Regulation and the Generation of Phenotypic Diversity

2019 ◽  
Vol 64 (1) ◽  
pp. 185-203 ◽  
Author(s):  
Karl M. Glastad ◽  
Brendan G. Hunt ◽  
Michael A.D. Goodisman
Keyword(s):  
Cellular Differentiation ◽  
Developmental Plasticity ◽  
Phenotypic Diversity ◽  
Epigenetic Inheritance ◽  
Evolutionary Significance ◽  
Epigenetic Information ◽  
Form And Function ◽  
Methylation Of Dna ◽  
Genome Regulation ◽  
And Function

Epigenetic inheritance is fundamentally important to cellular differentiation and developmental plasticity. In this review, we provide an introduction to the field of molecular epigenetics in insects. Epigenetic information is passed across cell divisions through the methylation of DNA, the modification of histone proteins, and the activity of noncoding RNAs. Much of our knowledge of insect epigenetics has been gleaned from a few model species. However, more studies of epigenetic information in traditionally nonmodel taxa will help advance our understanding of the developmental and evolutionary significance of epigenetic inheritance in insects. To this end, we also provide a brief overview of techniques for profiling and perturbing individual facets of the epigenome. Doing so in diverse cellular, developmental, and taxonomic contexts will collectively help shed new light on how genome regulation results in the generation of diversity in insect form and function.

Theheartstringsmutation in zebrafish causes heart/fin Tbx5 deficiency syndrome

Development ◽  
2002 ◽  
Vol 129 (19) ◽  
pp. 4635-4645 ◽  
Author(s):  
Deborah M. Garrity ◽  
Sarah Childs ◽  
Mark C. Fishman
Keyword(s):  
Large Family ◽  
Deficiency Syndrome ◽  
Heart Tube ◽  
Pectoral Fin ◽  
Lethal Mutant ◽  
Cardiac Defects ◽  
Form And Function ◽  
Whole Heart ◽  
And Function ◽  
Tbx5 Gene

Holt-Oram syndrome is one of the autosomal dominant human ‘heart-hand’ disorders, with a combination of upper limb malformations and cardiac defects. Holt-Oram syndrome is caused by mutations in the TBX5 gene, a member of a large family of T-box transcription factors that play important roles in cell-type specification and morphogenesis. In a screen for mutations affecting zebrafish cardiac function, we isolated the recessive lethal mutant heartstrings, which lacks pectoral fins and exhibits severe cardiac dysfunction, beginning with a slow heart rate and progressing to a stretched, non-functional heart.We mapped and cloned the heartstrings mutation and find it to encode the zebrafish ortholog of the TBX5 gene. The heartstrings mutation causes premature termination at amino acid 316. Homozygous mutant embryos never develop pectoral fin buds and do not express several markers of early fin differentiation. The total absence of any fin bud differentiation distinguishes heartstrings from most other mutations that affect zebrafish fin development, suggesting that Tbx5 functions very early in the pectoral fin induction pathway. Moderate reduction of Tbx5 by morpholino causes fin malformations, revealing an additional early requirement for Tbx5 in coordinating the axes of fin outgrowth. The heart of heartstrings mutant embryos appears to form and function normally through the early heart tube stage, manifesting only a slight bradycardia compared with wild-type siblings. However, the heart fails to loop and then progressively deteriorates, a process affecting the ventricle as well as the atrium.Relative to mammals, fish require lower levels of Tbx5 to produce malformed appendages and display whole-heart rather than atrial-predominant cardiac defects. However, the syndromic deficiencies of tbx5 mutation are remarkably well retained between fish and mammals.

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