Self‐differentiation and induction in the heart of Amblystoma

Bacon, Robert L.

doi:10.1002/jez.1400980202

Cited by 67 publications

(15 citation statements)

References 37 publications

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“…The above evidence, which is in accord with early observations of Bacon (1945) who showed that ectopic mesoderm differentiated into cardiac tissue after transplantation into the Amblystoma (urodele) foregut, suggests that endoderm that is associated with "cardiac" mesoderm at all stages of its developmental pathway secretes cardiac specification factors. However, this evidence must be classified as indirect because respecification, rather than direct specification of cardiac progenitor cells in situ, was observed in all of these experiments.…”

Section: Role Of Endoderm In Cardiac Myocyte Specificationsupporting

confidence: 80%

“…Concomitantly, the AL endoderm is transpositioned dorsomedially to establish the pharyngeal foregut endoderm. Although the proximity of the dorsal myocardium to the foregut endoderm is suggestive of a continuing inductive relationship between these tissues after formation of the definitive heart, this possibility has received little attention, despite early amphibian evidence indicating that foregut endoderm can induce cardiac tissue in ectopic mesoderm (Bacon, 1945). Recent unpublished findings using the avian model indicate that foregut endoderm signaling regulates development of the definitive heart.…”

Section: Perspectivesmentioning

confidence: 99%

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Endoderm and heart development

2000

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Section: Role Of Endoderm In Cardiac Myocyte Specificationsupporting

confidence: 80%

Section: Perspectivesmentioning

confidence: 99%

Endoderm and heart development

2000

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“…Isolated linear heart tubes from chick and amphibian embryos maintain their ability to form a dextral loop ex vivo 27,28 . We therefore hypothesized that in the absence of Nodal signalling, preferential dextral cardiac looping is maintained due to an alternative tissue-intrinsic mechanism.…”

Section: Resultsmentioning

confidence: 99%

A Nodal-independent and tissue-intrinsic mechanism controls heart-looping chirality

et al. 2013

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Breaking left-right symmetry in bilateria is a major event during embryo development that is required for asymmetric organ position, directional organ looping and lateralized organ function in the adult. Asymmetric expression of Nodal-related genes is hypothesized to be the driving force behind regulation of organ laterality. Here we identify a Nodal-independent mechanism that drives asymmetric heart looping in zebrafish embryos. In a unique mutant defective for the Nodal-related southpaw gene, preferential dextral looping in the heart is maintained, whereas gut and brain asymmetries are randomized. As genetic and pharmacological inhibition of Nodal signalling does not abolish heart asymmetry, a yet undiscovered mechanism controls heart chirality. This mechanism is tissue intrinsic, as explanted hearts maintain ex vivo retain chiral looping behaviour and require actin polymerization and myosin II activity. We find that Nodal signalling regulates actin gene expression, supporting a model in which Nodal signalling amplifies this tissue-intrinsic mechanism of heart looping.

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“…Received June 22, 2013;revised version accepted October 3, 2013. As early as the 1920s, it was realized that uncommitted mesodermal progenitors can be induced to form cardiac cells (Bacon 1945 and references therein), and subsequent embryological and stem cell studies led to the identification of numerous paracrine signals that promote cardiogenic differentiation (Noseda et al 2011). However, despite the intense interest in regenerating cardiomyocytes from pluripotent stem or adult progenitor cells, the extracellular signals and nuclear events that define cardiac commitment have remained obscure.…”

mentioning

confidence: 99%

Coordinate Nodal and BMP inhibition directs Baf60c-dependent cardiomyocyte commitment

et al. 2013

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A critical but molecularly uncharacterized step in heart formation and regeneration is the process that commits progenitor cells to differentiate into cardiomyocytes. Here, we show that the endoderm-derived dual Nodal/bone morphogenetic protein (BMP) antagonist Cerberus-1 (Cer1) in embryonic stem cell cultures orchestrates two signaling pathways that direct the SWI/SNF chromatin remodeling complex to cardiomyogenic loci in multipotent (KDR/Flk1 + ) progenitors, activating lineage-specific transcription. Transient inhibition of Nodal by Cer1 induces Brahma-associated factor 60c (Baf60c), one of three Baf60 variants (a, b, and c) that are mutually exclusively assembled into SWI/SNF. Blocking Nodal and BMP also induces lineage-specific transcription factors Gata4 and Tbx5, which interact with Baf60c. siRNA to Cer1, Baf60c, or the catalytic SWI/SNF subunit Brg1 prevented the developmental opening of chromatin surrounding the Nkx2.5 early cardiac enhancer and cardiomyocyte differentiation. Overexpression of Baf60c fully rescued these deficits, positioning Baf60c and SWI/ SNF function downstream from Cer1. Thus, antagonism of Nodal and BMP coordinates induction of the myogenic Baf60c variant and interacting transcription factors to program the developmental opening of cardiomyocytespecific loci in chromatin. This is the first demonstration that cues from the progenitor cell environment direct the subunit variant composition of SWI/SNF to remodel the transcriptional landscape for lineage-specific differentiation.

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Self‐differentiation and induction in the heart of Amblystoma

Cited by 67 publications

References 37 publications

Endoderm and heart development

Endoderm and heart development

A Nodal-independent and tissue-intrinsic mechanism controls heart-looping chirality

Coordinate Nodal and BMP inhibition directs Baf60c-dependent cardiomyocyte commitment

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