scholarly journals Multipotent cell lineages in early mouse development depend on SOX2 function

2003 ◽  
Vol 17 (1) ◽  
pp. 126-140 ◽  
Author(s):  
A. A. Avilion
Development ◽  
1993 ◽  
Vol 117 (2) ◽  
pp. 483-492 ◽  
Author(s):  
J.J. Brown ◽  
V.E. Papaioannou

The ontogeny of hyaluronan (HA) secretion during early mouse embryogenesis has been investigated using a biotin-labelled HA-binding complex from cartilage proteoglycan. HA is first secreted by visceral endoderm cells of the early egg cylinder on day 5.5 post coitum (p.c.), predominantly into the expanding yolk cavity. On day 6.5 p.c., HA is present in both the yolk and proamniotic cavities, but pericellular staining is restricted to the visceral endoderm and a population of embryonic ectoderm cells at the antimesometrial end of the proamniotic cavity. By the primitive streak stage, HA is secreted into the ectoplacental, exocoelomic, amniotic and yolk cavities, whilst the only cells exhibiting pericellular staining are those of the embryonic and extraembryonic mesoderm, including the allantois. Comparisons of HA-staining patterns of cultured whole blastocysts, microdissected trophectoderm fragments and immunosurgically isolated inner cell masses, revealed no trophoblast-associated HA secretion during outgrowth in vitro but significant synthetic activity by the endodermal derivatives of differentiating inner cell masses. To identify the cell lineages responsible for secretion of HA into the embryonic cavities and to investigate the origin of the HA observed around migrating mesoderm cells, day 7.5 p.c. primitive streak stage conceptuses were dissected into their various embryonic and extraembryonic cell lineages. HA secretion was observed after short-term suspension culture of mesoderm, embryonic ectoderm and embryonic endoderm, but was undetectable in fragments of ectoplacental cone, parietal yolk sac (primary giant trophoblast and parietal endoderm), extraembryonic ectoderm or extraembryonic endoderm. The level of synthesis by the HA-positive tissues was markedly enhanced by culture in medium containing serum, compared with that obtained following culture in medium supplemented with a defined serum substitute containing insulin, transferrin, selenous acid and linoleic acid. This suggests that additional growth factors, present in serum but absent from the serum substitute, are required for optimal HA synthesis by the HA-secreting tissues in vitro, and probably also in vivo. The implications of these events for implantation and the development of peri- and early post-implantation mouse embryos are discussed, and a new role for HA in the initial formation and expansion of the embryonic cavities is proposed.


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

2010 ◽  
Vol 42 (12) ◽  
pp. 1093-1100 ◽  
Author(s):  
Julie Borgel ◽  
Sylvain Guibert ◽  
Yufeng Li ◽  
Hatsune Chiba ◽  
Dirk Schübeler ◽  
...  

Development ◽  
2016 ◽  
Vol 143 (16) ◽  
pp. 2958-2964 ◽  
Author(s):  
Shin Kobayashi ◽  
Yusuke Hosoi ◽  
Hirosuke Shiura ◽  
Kazuo Yamagata ◽  
Saori Takahashi ◽  
...  

Development ◽  
2002 ◽  
Vol 129 (14) ◽  
pp. 3455-3468 ◽  
Author(s):  
Dominic P. Norris ◽  
Jane Brennan ◽  
Elizabeth K. Bikoff ◽  
Elizabeth J. Robertson

The TGFβ-related growth factor Nodal governs anteroposterior (AP) and left-right (LR) axis formation in the vertebrate embryo. A conserved intronic enhancer (ASE), containing binding sites for the fork head transcription factor Foxh1, modulates dynamic patterns of Nodal expression during early mouse development. This enhancer is responsible for early activation of Nodal expression in the epiblast and visceral endoderm, and at later stages governs asymmetric expression during LR axis formation. We demonstrate ASE activity is strictly Foxh1 dependent. Loss of this autoregulatory enhancer eliminates transcription in the visceral endoderm and decreases Nodal expression in the epiblast, but causes surprisingly discrete developmental abnormalities. Thus lowering the level of Nodal signaling in the epiblast disrupts both orientation of the AP axis and specification of the definitive endoderm. Targeted removal of the ASE also dramatically reduces left-sided Nodal expression, but the early events controlling LR axis specification are correctly initiated. However loss of the ASE disrupts Lefty2 (Leftb) expression and causes delayed Pitx2 expression leading to late onset, relatively minor LR patterning defects. The feedback loop is thus essential for maintenance of Nodal signals that selectively regulate target gene expression in a temporally and spatially controlled fashion in the mouse embryo.


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