Cell fate determination in embryonic ectoderm

Chang, Chenbei; Hemmati‐Brivanlou, Ali

doi:10.1002/(sici)1097-4695(199808)36:2<128::aid-neu3>3.0.co;2-3

Cited by 68 publications

(26 citation statements)

References 176 publications

(28 reference statements)

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“…All these genes can be upregulated by BMP4 and the overexpression of these factors in Xenopus results in ventralized phenotypes (i.e. promote epidermal differentiation at the expense of neural structures), as does BMP4 (Chang and Hemmati-Brivanlou, 1998 for a review). The expression is blocked by the inhibitors of BMP 4 signaling such as dominant negative type I BMP receptors.…”

Section: Transcriptional Regulation Of Epidermal and Neural Fates By mentioning

confidence: 99%

The choice between epidermal and neural fate: a matter of calcium.

Moreau

Leclerc²

2004

Int. J. Dev. Biol.

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The development of the vertebrate embryo, which includes the induction and the patterning of the three germ layers, requires signaling among cells. In vertebrates, cells of the embryonic ectoderm have a choice during gastrulation between two fates; they give rise to epidermal progenitors on the ventral side and neural progenitors on the dorsal side. It was first shown by Spemann and Mangold in 1924 that the dorsal mesoderm (also called the SpemannMangold Organizer) has a potent biological capacity to induce nervous system from the adjacent ectoderm. A similar observation was reported in amniotes, indicating that neural induction by the Organizer is a conserved process controlling the initial steps in vertebrates neurogenesis. Molecular studies of the last decade have led to the identification of signaling molecules which participate in these embryonic decisions. Epidermis induction occurs through a signaling cascade involving Bone Morphogenetic Proteins (BMP 2, 4, 7) and receptor-regulated Smad proteins which translocate into the nucleus to form active transcriptional complexes. These molecules mediate BMPs effect to activate epidermal-specific gene expression and to repress neural-specific gene transcription. Neural fate is revealed by factors secreted by the dorsal mesoderm (Noggin, Chordin, Follistatin, …) which act by blocking BMP signaling. Consequently, epidermal fate is an induced fate while neural fate is interpreted as a default state of the ectoderm. In this review, we describe the signaling pathways which act to determine the fate of the ectoderm and discuss an alternative model in which neural fate is not a default state. This new model integrates the activation of a calcium-dependent signaling pathway due to an influx of calcium through L-type calcium channels. In this model, calcium plays a central regulatory role. While calcium is required for neural determination, epidermal determination occurs when calcium-dependent signaling pathways are inactive.

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Section: Transcriptional Regulation Of Epidermal and Neural Fates By mentioning

confidence: 99%

The choice between epidermal and neural fate: a matter of calcium.

Moreau

Leclerc²

2004

Int. J. Dev. Biol.

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“…At the ectodermal level, BMP-4 behaves like a strong epidermal inducer in regions with low antagonist concentrations (ventral region of the ectoderm), while high levels of BMP-4 antagonists in the dorsal region induce the formation of the neuroectoderm during Xenopus development and probably more generally in vertebrate development. 2,3 For the ectoderm, this indirect and inhibitory mode of the dorsal organizer action is described in the 'neural default' model, according to which ectodermal cells will undergo neural differentiation unless instructed by BMPs not to do so, and to become epidermal. 2 Numerous studies in Xenopus laevis support this 'default' model to explain the neural cell fate determination.…”

Section: Introductionmentioning

confidence: 99%

BMP-4 induces a Smad-dependent apoptotic cell death of mouse embryonic stem cell-derived neural precursors

et al. 2005

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Embryonic ectoderm is fated to become either neural or epidermal, depending on patterning processes that occur before and during gastrulation. It has been stated that epidermal commitment proceeds from a bone morphogenetic protein-4 (BMP-4)-dependent inhibition of dorsal ectoderm neuralization. We recently demonstrated that murine embryonic stem (ES) cells treated with BMP-4 undergo effective keratinocyte commitment and epidermogenesis. Focusing on the precise role of BMP-4 in the early choice between neural and epidermal commitment, we show here that BMP-4 treatment of ES cells leads to a dramatic apoptotic death of Sox-1 þ neural precursors with concomitant epidermal engagement. In addition, neutralization of the Smad pathway prevents both the BMP-4 apoptotic process and the inhibition of neural differentiation. Our results suggest that, in mammals, BMP-4, as an active inducer of epidermal commitment, interferes with the survival of neural precursors through induction of their apoptotic cell death.

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“…Neuralizing factors secreted by the Spemann Organizer, including noggin, chordin, and follistatin, act by sequestering bone morphogenetic protein 4 (BMP-4), which otherwise would direct ectoderm toward an epidermal fate (2,3). Neural induction is therefore regarded as a default pathway (4).…”

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confidence: 99%

The Ca ² +-induced methyltransferase xPRMT1b controls neural fate in amphibian embryo

Batut

Vandel

Leclerc

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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We have previously shown that an increase in intracellular Ca 2؉ is both necessary and sufficient to commit ectoderm to a neural fate in Xenopus embryos. However, the relationship between this Ca 2؉ increase and the expression of early neural genes has yet to be defined. Using a subtractive cDNA library between untreated and caffeine-treated animal caps, i.e., control ectoderm and ectoderm induced toward a neural fate by a release of Ca 2؉ , we have isolated the arginine N-methyltransferase, xPRMT1b, a Ca 2؉ -induced target gene, which plays a pivotal role in this process. First, we show in embryo and in animal cap that xPRMT1b expression is Ca 2؉ -regulated. Second, overexpression of xPRMT1b induces the expression of early neural genes such as Zic3. Finally, in the whole embryo, antisense approach with morpholino oligonucleotide against xPRMT1b impairs neural development and in animal caps blocks the expression of neural markers induced by a release of internal Ca 2؉ . Our results implicate an instructive role of an enzyme, an arginine methyltransferase protein, in the embryonic choice of determination between epidermal and neural fate. The results presented provide insights by which a Ca 2؉ increase induces neural fate.calcium ͉ neural induction ͉ protein methyltransferase ͉ Xenopus

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Cell fate determination in embryonic ectoderm

Cited by 68 publications

References 176 publications

The choice between epidermal and neural fate: a matter of calcium.

The choice between epidermal and neural fate: a matter of calcium.

BMP-4 induces a Smad-dependent apoptotic cell death of mouse embryonic stem cell-derived neural precursors

The Ca ² +-induced methyltransferase xPRMT1b controls neural fate in amphibian embryo

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Cell fate determination in embryonic ectoderm

Cited by 68 publications

References 176 publications

The choice between epidermal and neural fate: a matter of calcium.

The choice between epidermal and neural fate: a matter of calcium.

BMP-4 induces a Smad-dependent apoptotic cell death of mouse embryonic stem cell-derived neural precursors

The Ca 2 +-induced methyltransferase xPRMT1b controls neural fate in amphibian embryo

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The Ca ² +-induced methyltransferase xPRMT1b controls neural fate in amphibian embryo