The mouse fetal‐placental arterial connection: A paradigm involving the primitive streak and visceral endoderm with implications for human development

2019 ◽  
Vol 9 (2) ◽  
Author(s):  
Karen M. Downs ◽  
Adriana M. Rodriguez
Keyword(s):  
Human Development ◽  
Primitive Streak ◽  
Visceral Endoderm

scholarly journals Correct Patterning of the Primitive Streak Requires the Anterior Visceral Endoderm

PLoS ONE ◽  
2011 ◽  
Vol 6 (3) ◽  
pp. e17620 ◽  
Author(s):  
Daniel W. Stuckey ◽  
Aida Di Gregorio ◽  
Melanie Clements ◽  
Tristan A. Rodriguez
Keyword(s):  
Primitive Streak ◽  
Visceral Endoderm ◽  
Anterior Visceral Endoderm

scholarly journals Characterizing the Emergence of Liver and Gallbladder from the Embryonic Endoderm through Single-Cell RNA-Seq

2019 ◽  
Author(s):  
Tianhao Mu ◽  
Liqin Xu ◽  
Yu Zhong ◽  
Xinyu Liu ◽  
Zhikun Zhao ◽  
...  
Keyword(s):  
Single Cell ◽  
Primitive Streak ◽  
Developmental Trajectory ◽  
Visceral Endoderm ◽  
Rna Seq ◽  
Internal Organs ◽  
Factors Associated ◽  
Complex Signaling ◽  
Foregut Endoderm ◽  
Mesenchymal Epithelial Transition

AbstractThe liver and gallbladder are among the most important internal organs derived from the endoderm. Several inductive signals regulate liver development, yet the pure nascent hepatic and gallbladder cells are unable to be isolated due to limited cell markers and cell numbers. The transcriptome networks of the hepatic lineage in the endoderm, and how the gallbladder differentiates from the adjacent endoderm population, are not fully understood. Using a transgenic Foxa2eGFP reporter mouse line, we performed deep single-cell RNA sequencing on 1,966 individual cells, including nascent hepatic and gallbladder cells, isolated from the endoderm and hepatic regions from ten embryonic stages, ranging from day E7.5 to E15.5. We identified the embryonic liver developmental trajectory from primitive streak to hepatoblasts and characterized the transcriptome of the hepatic lineage. During pre-hepatogenesis (5-6 somite stage), we have identified two groups of foregut endoderm cells, one derived from visceral endoderm and the second derived from primitive streak via a mesenchymal-epithelial transition (MET). During the liver specification stages, liver primordium was identified to share both foregut and liver features. We also documented dynamic gene expression during the epithelial-hepatic transition (EHT). Six gene groups were found to switch on or off at different stages during liver specification. Importantly, we found that RXR complex signaling and newly identified transcription factors associated with liver specification. Moreover, we revealed the gallbladder primordium cells at E9.5 and found genes that transcriptionally distinguish them from the liver primordium. The present data provides a high-resolution resource and critical insights for understanding the emergence of the endoderm, liver and gallbladder development.

HNF3beta and Lim1 interact in the visceral endoderm to regulate primitive streak formation and anterior-posterior polarity in the mouse embryo

Development ◽  
1999 ◽  
Vol 126 (20) ◽  
pp. 4499-4511 ◽  
Author(s):  
A. Perea-Gomez ◽  
W. Shawlot ◽  
H. Sasaki ◽  
R.R. Behringer ◽  
S. Ang
Keyword(s):  
Mouse Embryo ◽  
Primitive Streak ◽  
Axis Formation ◽  
Visceral Endoderm ◽  
Primary Defect ◽  
Homozygous Mutant ◽  
Early Mouse ◽  
Mesoderm Patterning ◽  
Anterior Posterior ◽  
Anterior Visceral Endoderm

Recent embryological and genetic experiments have suggested that the anterior visceral endoderm and the anterior primitive streak of the early mouse gastrula function as head- and trunk-organising centers, respectively. Here, we report that HNF3beta and Lim1 are coexpressed in both organising centers suggesting synergistic roles of these genes in regulating organiser functions and hence axis development in the mouse embryo. To investigate this possibility, we generated compound HNF3beta and Lim1 mutant embryos. An enlarged primitive streak and a lack of axis formation were observed in HNF3beta (−)(/)(−);Lim1(−)(/)(−), but not in single homozygous mutant embryos. Chimera experiments indicate that the primary defect in these double homozygous mutants is due to loss of activity of HNF3beta and Lim1 in the visceral endoderm. Altogether, these data provide evidence that these genes function synergistically to regulate organiser activity of the anterior visceral endoderm. Moreover, HNF3beta (−)(/)(−);Lim1(−)(/)(−) mutant embryos also exhibit defects in mesoderm patterning that are likely due to lack of specification of anterior primitive streak cells.

Reconciling different models of forebrain induction and patterning: a dual role for the hypoblast

Development ◽  
2000 ◽  
Vol 127 (17) ◽  
pp. 3839-3854 ◽  
Author(s):  
A.C. Foley ◽  
I. Skromne ◽  
C.D. Stern
Keyword(s):  
Nervous System ◽  
Molecular Markers ◽  
Regional Identity ◽  
Neural Tissue ◽  
Primitive Streak ◽  
Dual Role ◽  
Visceral Endoderm ◽  
Forebrain Development ◽  
Early Markers

Several models have been proposed for the generation of the rostral nervous system. Among them, Nieuwkoop's activation/transformation hypothesis and Spemann's idea of separate head and trunk/tail organizers have been particularly favoured recently. In the mouse, the finding that the visceral endoderm (VE) is required for forebrain development has been interpreted as support for the latter model. Here we argue that the chick hypoblast is equivalent to the mouse VE, based on fate, expression of molecular markers and characteristic anterior movements around the time of gastrulation. We show that the hypoblast does not fit the criteria for a head organizer because it does not induce neural tissue from naive epiblast, nor can it change the regional identity of neural tissue. However, the hypoblast does induce transient expression of the early markers Sox3 and Otx2. The spreading of the hypoblast also directs cell movements in the adjacent epiblast, such that the prospective forebrain is kept at a distance from the organizer at the tip of the primitive streak. We propose that this movement is important to protect the forebrain from the caudalizing influence of the organizer. This dual role of the hypoblast is more consistent with the Nieuwkoop model than with the notion of separate organizers, and accommodates the available data from mouse and other vertebrates.

Head induction in the chick by primitive endoderm of mammalian, but not avian origin

Development ◽  
1999 ◽  
Vol 126 (4) ◽  
pp. 815-825 ◽  
Author(s):  
H. Knoetgen ◽  
C. Viebahn ◽  
M. Kessel
Keyword(s):  
Lower Layer ◽  
Homeobox Gene ◽  
Primitive Streak ◽  
Neural Plate ◽  
Visceral Endoderm ◽  
Avian Origin ◽  
Bmp Antagonist ◽  
Rabbit Embryos ◽  
Inductive Potential ◽  
Anterior Visceral Endoderm

Different types of endoderm, including primitive, definitive and mesendoderm, play a role in the induction and patterning of the vertebrate head. We have studied the formation of the anterior neural plate in chick embryos using the homeobox gene GANF as a marker. GANF is first expressed after mesendoderm ingression from Hensen's node. We found that, after transplantation, neither the avian hypoblast nor the anterior definitive endoderm is capable of GANF induction, whereas the mesendoderm (young head process, prechordal plate) exhibits a strong inductive potential. GANF induction cannot be separated from the formation of a proper neural plate, which requires an intact lower layer and the presence of the prechordal mesendoderm. It is inhibited by BMP4 and promoted by the presence of the BMP antagonist Noggin. In order to investigate the inductive potential of the mammalian visceral endoderm, we used rabbit embryos which, in contrast to mouse embryos, allow the morphological recognition of the prospective anterior pole in the living, pre-primitive-streak embryo. The anterior visceral endoderm from such rabbit embryos induced neuralization and independent, ectopic GANF expression domains in the area pellucida or the area opaca of chick hosts. Thus, the signals for head induction reside in the anterior visceral endoderm of mammals whereas, in birds and amphibia, they reside in the prechordal mesendoderm, indicating a heterochronic shift of the head inductive capacity during the evolution of mammalia.

Isolation of differentially expressed human cDNA clones: similarities between mouse and human embryonal carcinoma cell differentiation

Development ◽  
1988 ◽  
Vol 104 (3) ◽  
pp. 403-413
Author(s):  
M.V. Wiles
Keyword(s):  
Cell Differentiation ◽  
Human Development ◽  
Cell Line ◽  
Cdna Library ◽  
Embryonal Carcinoma ◽  
Cdna Clones ◽  
Embryonal Carcinoma Cell ◽  
Visceral Endoderm ◽  
Induced Differentiation ◽  
Ec Cells

The study of early human development is of great importance but has been limited by the lack of suitable reagents. Recently, however, the human embryonal carcinoma (EC) cell line NT2D1 has been isolated. This cell line will differentiate upon exposure to retinoic acid (RA). A cDNA library was constructed from poly(A)+ RNA derived from NT2D1 cells treated with 10(−5) M-RA for 7 days (delta NT2D1 cells). By differential cDNA screening, it was found that 1.12% of delta NT2D1 cDNA recombinants screened detected an increase in signal with 32P-cDNAs derived from delta NT2D1 as compared with NT2D1. To compare RA-induced differentiation of mouse and human EC cells, the delta NT2D1 cDNA library was rescreened with 32P-cDNAs derived from the mouse EC cell line F9 and the result compared with 32P-cDNA derived from F9 differentiated to parietalendoderm (F9PE)-like cells and visceral-endoderm (F9VE)-like cells. Approximately 1.2% of the delta NT2D1 cDNA recombinants detected a differential increase in signal following differentiation of mouse EC cells to F9VE and/or F9PE. Of these homologous regulated sequences, 0.3% were common to both mouse and human EC cell RA-induced differentiation. Five different cDNA clones were isolated that detect a marked increase (5- to 75-fold) in mRNA abundance following RA-induced differentiation of NT2D1. Of these five clones, three detect homologous mRNAs which also increase in abundance following differentiation of the mouse EC cell line F9 to PE- and/or VE-like cells; the other two clones do not detect sequences in the mouse mRNAs tested. One clone shows homology to SPARC, a gene known to be regulated during mouse embryonic development. While another clone, SO5A, has a limited range of expression, being detected in F9VE and in a human parietal-endoderm-like cell, but not in F9PE and a human visceral-endoderm-like cell. This work shows that there are both similarities and differences in mouse and human EC cell differentiation, and these cDNA clones provide some of the first reagents for studying the molecular biology of human development.

scholarly journals Transcriptional Regulator BPTF/FAC1 Is Essential for Trophoblast Differentiation during Early Mouse Development

2008 ◽  
Vol 28 (22) ◽  
pp. 6819-6827 ◽  
Author(s):  
Tobias Goller ◽  
Franz Vauti ◽  
Suresh Ramasamy ◽  
Hans-Henning Arnold
Keyword(s):  
Subsequent Development ◽  
Transcriptional Regulator ◽  
Primitive Streak ◽  
Embryonic Lethality ◽  
Visceral Endoderm ◽  
Loss Of Function ◽  
Mouse Development ◽  
Trophoblast Stem Cells ◽  
Early Mouse ◽  
Ectoplacental Cone

ABSTRACT The putative transcriptional regulator BPTF/FAC1 is expressed in embryonic and extraembryonic tissues of the early mouse conceptus. The extraembryonic trophoblast lineage in mammals is essential to form the fetal part of the placenta and hence for the growth and viability of the embryo in utero. Here, we describe a loss-of-function allele of the BPTF/FAC1 gene that causes embryonic lethality in the mouse. BPTF/FAC1-deficient embryos form apparently normal blastocysts that implant and develop epiblast, visceral endoderm, and extraembryonic ectoderm including trophoblast stem cells. Subsequent development of mutants, however, is arrested at the early gastrula stage (embryonic day 6.5), and virtually all null embryos die before midgestation. Most notably, the ectoplacental cone is drastically reduced or absent in mutants, which may cause the embryonic lethality. Development of the mutant epiblast is also affected, as the anterior visceral endoderm and the primitive streak do not form correctly, while brachyury-expressing mesodermal cells arise but are delayed. The mutant phenotype suggests that gastrulation is initiated, but no complete anteroposterior axis of the epiblast appears. We conclude that BPTF/FAC1 is essential in the extraembryonic lineage for correct development of the ectoplacental cone and fetomaternal interactions. In addition, BPTF/FAC1 may also play a role either directly or indirectly in anterior-posterior patterning of the epiblast.

Otx2 is required for visceral endoderm movement and for the restriction of posterior signals in the epiblast of the mouse embryo

Development ◽  
2001 ◽  
Vol 128 (5) ◽  
pp. 753-765 ◽  
Author(s):  
A. Perea-Gomez ◽  
K.A. Lawson ◽  
M. Rhinn ◽  
L. Zakin ◽  
P. Brulet ◽  
...  
Keyword(s):  
Essential Role ◽  
Homeobox Gene ◽  
Primitive Streak ◽  
Lineage Tracing ◽  
Secreted Proteins ◽  
Visceral Endoderm ◽  
Cellular Mechanisms ◽  
Cell Fates ◽  
Marker Studies ◽  
Anterior Visceral Endoderm

Genetic and embryological experiments have demonstrated an essential role for the visceral endoderm in the formation of the forebrain; however, the precise molecular and cellular mechanisms of this requirement are poorly understood. We have performed lineage tracing in combination with molecular marker studies to follow morphogenetic movements and cell fates before and during gastrulation in embryos mutant for the homeobox gene Otx2. Our results show, first, that Otx2 is not required for proliferation of the visceral endoderm, but is essential for anteriorly directed morphogenetic movement. Second, molecules that are normally expressed in the anterior visceral endoderm, such as Lefty1 and Mdkk1, are not expressed in Otx2 mutants. These secreted proteins have been reported to antagonise, respectively, the activities of Nodal and Wnt signals, which have a role in regulating primitive streak formation. The visceral endoderm defects of the Otx2 mutants are associated with abnormal expression of primitive streak markers in the epiblast, suggesting that anterior epiblast cells acquire primitive streak characteristics. Taken together, our data support a model whereby Otx2 functions in the anterior visceral endoderm to influence the ability of the adjacent epiblast cells to differentiate into anterior neurectoderm, indirectly, by preventing them from coming under the influence of posterior signals that regulate primitive streak formation.

scholarly journals Visceral endoderm-restricted translation of Otx1 mediates recovery of Otx2 requirements for specification of anterior neural plate and normal gastrulation

Development ◽  
1998 ◽  
Vol 125 (24) ◽  
pp. 5091-5104 ◽  
Author(s):  
D. Acampora ◽  
V. Avantaggiato ◽  
F. Tuorto ◽  
P. Briata ◽  
G. Corte ◽  
...  
Keyword(s):  
Transcriptional Control ◽  
Expression Patterns ◽  
Epileptic Seizures ◽  
Primitive Streak ◽  
Neural Plate ◽  
Visceral Endoderm ◽  
Temporal Expression ◽  
Biochemical Activity ◽  
The Difference ◽  
Anterior Neural Plate

Otx1 and Otx2, two murine homologs of the Drosophila orthodenticle (otd) gene, contribute to brain morphogenesis. In particular Otx1 null mice are viable and show spontaneous epileptic seizures and abnormalities affecting the dorsal telencephalic cortex. Otx2 null mice die early in development and fail in specification of the rostral neuroectoderm and proper gastrulation. In order to determine whether Otx1(−/−)and Otx2(−/−) highly divergent phenotypes reflect differences in temporal expression or biochemical activity of OTX1 and OTX2 proteins, the Otx2-coding sequence was replaced by a human Otx1 full-coding cDNA. Homozygous mutant embryos recovered anterior neural plate and proper gastrulation but failed to maintain forebrain-midbrain identities, displaying a headless phenotype from 9 days post coitum (d.p.c.) onwards. Unexpectedly, in spite of the RNA distribution in both visceral endoderm (VE) and epiblast, the hOTX1 protein was synthesized only in the VE. This VE-restricted translation was sufficient to recover Otx2 requirements for specification of the anterior neural plate and proper organization of the primitive streak, thus providing evidence that the difference between Otx1 and Otx2 null mice phenotypes originates from their divergent expression patterns. Moreover, our data lead us to hypothesize that the differential post-transcriptional control existing between VE and epiblast cells may potentially contribute to fundamental regulatory mechanisms required for head specification.

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