Faculty Opinions recommendation of BMP signalling inhibits premature neural differentiation in the mouse embryo.

Author(s):  
James Briscoe
Development ◽  
2007 ◽  
Vol 134 (18) ◽  
pp. 3359-3369 ◽  
Author(s):  
A. Di-Gregorio ◽  
M. Sancho ◽  
D. W. Stuckey ◽  
L. A. Crompton ◽  
J. Godwin ◽  
...  

2006 ◽  
Vol 295 (2) ◽  
pp. 743-755 ◽  
Author(s):  
Anne Camus ◽  
Aitana Perea-Gomez ◽  
Anne Moreau ◽  
Jérôme Collignon

2012 ◽  
Vol 241 (11) ◽  
pp. 1808-1815 ◽  
Author(s):  
Beatriz Lopez-Escobar ◽  
Beatriz De Felipe ◽  
Jose Antonio Sanchez-Alcazar ◽  
Takako Sasaki ◽  
Andrew J. Copp ◽  
...  

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Sarah J. L. Graham ◽  
Krzysztof B. Wicher ◽  
Agnieszka Jedrusik ◽  
Guoji Guo ◽  
Wishva Herath ◽  
...  

eLife ◽  
2013 ◽  
Vol 2 ◽  
Author(s):  
Mattias Malaguti ◽  
Paul A Nistor ◽  
Guillaume Blin ◽  
Amy Pegg ◽  
Xinzhi Zhou ◽  
...  

Bone morphogenic protein (BMP) signalling contributes towards maintenance of pluripotency and favours mesodermal over neural fates upon differentiation, but the mechanisms by which BMP controls differentiation are not well understood. We report that BMP regulates differentiation by blocking downregulation of Cdh1, an event that accompanies the earliest stages of neural and mesodermal differentiation. We find that loss of Cdh1 is a limiting requirement for differentiation of pluripotent cells, and that experimental suppression of Cdh1 activity rescues the BMP-imposed block to differentiation. We further show that BMP acts prior to and independently of Cdh1 to prime pluripotent cells for mesoderm differentiation, thus helping to reinforce the block to neural differentiation. We conclude that differentiation depends not only on exposure to appropriate extrinsic cues but also on morphogenetic events that control receptivity to those differentiation cues, and we explain how a key pluripotency signal, BMP, feeds into this control mechanism.


Development ◽  
1998 ◽  
Vol 125 (8) ◽  
pp. 1447-1456 ◽  
Author(s):  
D. Onichtchouk ◽  
A. Glinka ◽  
C. Niehrs

Xvent-1 and Xvent-2 are members of a novel homeobox subfamily that have been implicated in dorsoventral patterning in Xenopus mesoderm and are thought to function in BMP signalling. Here we investigate the requirement for Xvent function by employing two dominant-negative strategies. Loss of Xvent function dorsalizes ventral mesoderm, induces secondary embryonic axes and directly neuralizes ectoderm. We further find that (1) Xvents act as transcriptional repressors, (2) Xvents function in an additive fashion and (3) a surprising number of genes are able to rescue dominant-negative Xvent phenotypes including Bmp-4, Smad-1 and wild-type Xvents and Xhox3, but not Xwnt-8. The results show that Xvent-1 and Xvent-2 are essential for ventral mesoderm formation and for preventing neural differentiation. A model is suggested to explain how Bmp-4 positional information is converted into distinct cellular responses.


Open Biology ◽  
2012 ◽  
Vol 2 (3) ◽  
pp. 120030 ◽  
Author(s):  
Ruth M. Arkell ◽  
Patrick P. L. Tam

The generation of an embryonic body plan is the outcome of inductive interactions between the progenitor tissues that underpin their specification, regionalization and morphogenesis. The intercellular signalling activity driving these processes is deployed in a time- and site-specific manner, and the signal strength must be precisely controlled. Receptor and ligand functions are modulated by secreted antagonists to impose a dynamic pattern of globally controlled and locally graded signals onto the tissues of early post-implantation mouse embryo. In response to the WNT, Nodal and Bone Morphogenetic Protein (BMP) signalling cascades, the embryo acquires its body plan, which manifests as differences in the developmental fate of cells located at different positions in the anterior–posterior body axis. The initial formation of the anterior (head) structures in the mouse embryo is critically dependent on the morphogenetic activity emanating from two signalling centres that are juxtaposed with the progenitor tissues of the head. A common property of these centres is that they are the source of antagonistic factors and the hub of transcriptional activities that negatively modulate the function of WNT, Nodal and BMP signalling cascades. These events generate the scaffold of the embryonic head by the early-somite stage of development. Beyond this, additional tissue interactions continue to support the growth, regionalization, differentiation and morphogenesis required for the elaboration of the structure recognizable as the embryonic head.


Author(s):  
Elizabeth S. Priori ◽  
T. Shigematsu ◽  
B. Myers ◽  
L. Dmochowski

Spontaneous release of type C virus particles in long-term cultures of mouse embryo cells as well as induction of similar particles in mouse embryo cell cultures with IUDR or BUDR have been reported. The presence of type C virus particles in cultures of normal rat embryos has not been reported.NB-1, a culture derived from embryos of a New Zealand Black (NB) rat (rats obtained from Mr. Samuel M. Poiley, N.C.I., Bethesda, Md.) and grown in McCoy's 5A medium supplemented with 20% fetal calf serum was passaged weekly. Extracellular virus particles similar to murine leukemia particles appeared in the 22nd subculture. General appearance of cells in passage 23 is shown in Fig. 1. Two budding figures and one immature type C virus particle may be seen in Fig. 2. The virus particles and budding were present in all further passages examined (currently passage 39). Various stages of budding are shown in Figs. 3a,b,c,d. Appearance of a mature virus particle is shown in Fig. 4.


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