Ligne primitive

Résumé

La ligne primitive apparaît lors de la gastrulation. Il s'agit d'un épaississement cellulaire se formant sur la face dorsale du disque embryonnaire, s'étendant sur les deux tiers de sa longueur. Cette ligne détermine l'axe longitudinal de l'embryon. Les cellules s'enfoncent au niveau de la ligne primitive pour former les trois couches cellulaires desquelles dériveront tous les organes : l'endoderme, le mésoderme et l'ectoderme. Le mésoderme se formera directement sous la ligne primitive en avant du Nœud de Hensen de part et d'autre d'un tube, l'axe organisateur, appelé notochorde. Notes et références Catégorie:Embryologie

Source officielle

https://fr.wikipedia.org/wiki/Ligne_primitive

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Tissue engineering is an interdisciplinary field that broadly impacts human health. This course provides students an overview of how engineering approaches can be used to investigate and manipulate cell and tissue functions and enable students to be on the cutting edge of tissue engineering.

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Differential impact of TGF beta/SMAD signaling activity elicited by Activin A and Nodal on endoderm differentiation of epiblast stem cells

Pierre Osteil

Allocation of cells to an endodermal fate in the gastrulating embryo is driven by Nodal signaling and consequent activation of TGF beta pathway. In vitro methodologies striving to recapitulate the process of endoderm differentiation, however, use TGF beta family member Activin in place of Nodal. This is despite Activin not known to have an in vivo role in endoderm differentiation. In this study, five epiblast stem cell lines were subjected to directed differentiation using both Activin A and Nodal to induce endodermal fate. A reporter line harboring endoderm markers FoxA2 and Sox17 was further analyzed for TGF beta pathway activation and WNT response. We demonstrated that Activin A-treated cells remain more primitive streak-like when compared to Nodal-treated cells that have a molecular profile suggestive of more advanced differentiation. Activin A elicited a robust TGF beta/SMAD activity, enhanced WNT signaling activity and promoted the generation of DE precursors. Nodal treatment resulted in lower TGF beta/SMAD activity, and a weaker, sustained WNT response, and ultimately failed to upregulate endoderm markers. This is despite signaling response resembling more closely the activity seen in vivo. These findings emphasize the importance of understanding the downstream activities of Activin A and Nodal signaling in directing in vitro endoderm differentiation of primed-state epiblast stem cells.

WILEY2022

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Epiblast-specific loss of HCF-1 leads to failure in anterior-posterior axis specification

Sylvain Frédéric Bessonnard, Daniel Constam, Winship Herr

Mammalian Host-Cell Factor 1 (HCF-1), a transcriptional co-regulator, plays important roles during the cell-division cycle in cell culture, embryogenesis as well as adult tissue. In mice, HCF-1 is encoded by the X-chromosome-linked Hcfc1 gene. Induced Hcfc1(cKO/+) heterozygosity with a conditional knockout (cKO) allele in the epiblast of female embryos leads to a mixture of HCF-1-positive and -deficient cells owing to random X-chromosome inactivation. These embryos survive owing to the replacement of all HCF-1-deficient cells by HCF-1-positive cells during E5.5 to E8.5 of development. In contrast, complete epiblast-specific loss of HCF-1 in male embryos, Hcfc1(epiko/Y), leads to embryonic lethality. Here, we characterize this lethality. We show that male epiblast-specific loss of Hcfc1 leads to a developmental arrest at E6.5 with a rapid progressive cell-cycle exit and an associated failure of anterior visceral endoderm migration and primitive streak formation. Subsequently, gastrulation does not take place. We note that the pattern of Hcfc1(epiKO/y) lethality displays many similarities to loss of beta-catenin function. These results reveal essential new roles for HCF-1 in early embryonic cell proliferation and development. (C) 2016 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license.

Academic Press Inc Elsevier Science2016

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Nodal specifies embryonic visceral endoderm and sustains pluripotent cells in the epiblast before overt axial patterning

Daniel Constam

Anteroposterior (AP) polarity in the mammalian embryo is specified during gastrulation when naive progenitor cells in the primitive ectoderm are recruited into the primitive streak to form mesoderm and endoderm. At the opposite pole, this process is inhibited by signals previously induced in distal visceral endoderm (DVE). Both DVE and primitive streak formation, and hence positioning of the AP axis, rely on the TGFbeta family member Nodal and its proprotein convertases Furin and Pace4. Here, we show that Nodal and Furin are initially co-expressed in the primitive endoderm together with a subset of DVE markers such as Lefty1 and Hex. However, with the appearance of extra-embryonic ectoderm (ExE), DVE formation is transiently inhibited. During this stage, Nodal activity is essential to specify embryonic VE and restrict the expression of Furin to the extra-embryonic region. Activation of Nodal is also necessary to maintain determinants of pluripotency such as Oct4, Nanog and Foxd3 during implantation, and to stimulate elongation of the egg cylinder, before inducing DVE and germ layer formation. We conclude that Nodal is already activated in primitive endoderm, but induces a functional DVE only after promoting the expansion of embryonic VE and pluripotent progenitor cells in the epiblast.

2006

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