scholarly journals Notch Signaling Commits Mesoderm to the Cardiac Lineage

2020 ◽  
Author(s):  
Evan S. Bardot ◽  
Bharati Jadhav ◽  
Nadeera Wickramasinghe ◽  
Amélie Rezza ◽  
Michael Rendl ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Heart Development ◽  
Cardiomyocyte Differentiation ◽  
Mouse Development ◽  
Mesoderm Specification ◽  
Cardiac Lineage ◽  
Underlying Mechanisms ◽  
Early Mouse ◽  
Differentiation Efficiency ◽  
Cardiac Mesoderm

AbstractDuring development multiple progenitor populations contribute to the formation of the four-chambered heart and its diverse lineages. However, the underlying mechanisms that result in the specification of these progenitor populations are not yet fully understood. We have previously identified a population of cells that gives rise selectively to the heart ventricles but not the atria. Here, we have used this knowledge to transcriptionally profile subsets of cardiac mesoderm from the mouse embryo and have identified an enrichment for Notch signaling components in ventricular progenitors. Using directed differentiation of human pluripotent stem cells, we next investigated the role of Notch in cardiac mesoderm specification in a temporally controlled manner. We show that transient Notch induction in mesoderm increases cardiomyocyte differentiation efficiency, while maintaining cardiomyocytes in an immature state. Finally, our data suggest that Notch interacts with WNT to enhance commitment to the cardiac lineage. Overall, our findings support the notion that key signaling events during early heart development are critical for proper lineage specification and provide evidence for early roles of Notch and WNT during mouse and human heart development.Summary statementEarly fate decisions are dictated by the embryonic signaling environment. We show that Notch signaling is active during early mouse development and that activating Notch in human cardiac mesoderm enhances cardiomyocyte differentiation efficiency.

scholarly journals Normal Immune System Development in Mice Lacking the Deltex-1 RING Finger Domain

2005 ◽  
Vol 25 (4) ◽  
pp. 1437-1445 ◽  
Author(s):  
Sébastien Storck ◽  
Frédéric Delbos ◽  
Nicolas Stadler ◽  
Catherine Thirion-Delalande ◽  
Florence Bernex ◽  
...  
Keyword(s):  
B Cell ◽  
Notch Signaling ◽  
Ubiquitin Ligase ◽  
Cell Lineage ◽  
Ring Finger ◽  
Mouse Development ◽  
Ring Finger Domain ◽  
Ubiquitin Ligase Activity ◽  
Immune System Development ◽  
Cell Commitment

ABSTRACT The Notch signaling pathway controls several cell fate decisions during lymphocyte development, from T-cell lineage commitment to the peripheral differentiation of B and T lymphocytes. Deltex-1 is a RING finger ubiquitin ligase which is conserved from Drosophila to humans and has been proposed to be a regulator of Notch signaling. Its pattern of lymphoid expression as well as gain-of-function experiments suggest that Deltex-1 regulates both B-cell lineage and splenic marginal-zone B-cell commitment. Deltex-1 was also found to be highly expressed in germinal-center B cells. To investigate the physiological function of Deltex-1, we generated a mouse strain lacking the Deltex-1 RING finger domain, which is essential for its ubiquitin ligase activity. Deltex-1Δ/Δ mice were viable and fertile. A detailed histological analysis did not reveal any defects in major organs. T- and B-cell development was normal, as were humoral responses against T-dependent and T-independent antigens. These data indicate that the Deltex-1 ubiquitin ligase activity is dispensable for mouse development and immune function. Possible compensatory mechanisms, in particular those from a fourth Deltex gene identified during the course of this study, are also discussed.

scholarly journals 03-P119 Decipher β-catenin functions in early mouse development

2009 ◽  
Vol 126 ◽  
pp. S101-S102
Author(s):  
Stefan Rudloff ◽  
Rolf Kemler
Keyword(s):  
Mouse Development ◽  
Early Mouse

Targets and dynamics of promoter DNA methylation during early mouse development

2010 ◽  
Vol 42 (12) ◽  
pp. 1093-1100 ◽  
Author(s):  
Julie Borgel ◽  
Sylvain Guibert ◽  
Yufeng Li ◽  
Hatsune Chiba ◽  
Dirk Schübeler ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Mouse Development ◽  
Promoter Dna Methylation ◽  
Promoter Dna ◽  
Early Mouse

scholarly journals Live imaging of X chromosome reactivation dynamics in early mouse development can discriminate naïve from primed pluripotent stem cells

Development ◽  
2016 ◽  
Vol 143 (16) ◽  
pp. 2958-2964 ◽  
Author(s):  
Shin Kobayashi ◽  
Yusuke Hosoi ◽  
Hirosuke Shiura ◽  
Kazuo Yamagata ◽  
Saori Takahashi ◽  
...  
Keyword(s):  
Stem Cells ◽  
X Chromosome ◽  
Pluripotent Stem Cells ◽  
Live Imaging ◽  
Mouse Development ◽  
Early Mouse

Overexpression of the tinman-related genes XNkx-2.5 and XNkx-2.3 in Xenopus embryos results in myocardial hyperplasia

Development ◽  
1996 ◽  
Vol 122 (11) ◽  
pp. 3549-3556 ◽  
Author(s):  
O.B. Cleaver ◽  
K.D. Patterson ◽  
P.A. Krieg
Keyword(s):  
Heart Development ◽  
Homeobox Gene ◽  
Cardiac Differentiation ◽  
Myocardial Cells ◽  
Differentiation Markers ◽  
Heart Field ◽  
Cardiac Mesoderm ◽  
Xenopus Laevis Embryos ◽  
Functional Homologues

Drosophila tinman is an NK-class homeobox gene required for formation of the dorsal vessel, the insect equivalent of the vertebrate heart. Vertebrate sequences related to tinman, such as mouse Nkx-2.5, chicken cNkx-2.5, Xenopus XNkx-2.5 and XNkx-2.3 are expressed in cardiac precursors and in tissues involved in induction of cardiac mesoderm. Mice which lack a functional Nkx-2.5 gene die due to cardiac defects. To determine the role of tinman-related sequences in heart development, we have overexpressed both XNkx-2.3 and XNkx-2.5 in Xenopus laevis embryos. The resulting embryos are morphologically normal except that they have enlarged hearts. The enlarged heart phenotype is due to a thickening of the myocardium caused by an increase in the overall number of myocardial cells (hyperplasia). Neither ectopic nor precocious expression of cardiac differentiation markers is detectable in overexpressing embryos. These results suggest that both XNkx-2.3 and XNkx-2.5 are functional homologues of tinman, responsible for maintenance of the heart field.

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