Retinoic acid receptors and cellular retinoid binding proteins. II. Their differential pattern of transcription during early morphogenesis in mouse embryos

Development ◽  
1991 ◽  
Vol 111 (1) ◽  
pp. 45-60 ◽  
Author(s):  
E. Ruberte ◽  
P. Dolle ◽  
P. Chambon ◽  
G. Morriss-Kay

In situ hybridization with 35S-labelled RNA probes was used to study the distribution of transcripts of genes coding for the retinoic acid receptors, RAR-alpha, -beta and -gamma, and the cellular binding proteins for retinoic acid (CRABP I) and retinol (CRBP I), in mouse embryos during the period of early morphogenesis. Primary mesenchyme formation was associated with CRBP I labelling of both epiblast and mesenchyme of the primitive streak, while the CRABP probe labelled the migrating primary mesenchyme cells. Neural crest cell emigration and migration were associated with CRABP labelling of both neural epithelium (excluding the floor plate) and neural crest cells, while CRBP I expression was restricted to basal and apical regions of the epithelium (excluding the floor plate). The strongest neuroepithelial signal for CRABP was in the preoptic hindbrain. RAR-beta was present in presomitic stage embryos, being expressed at highest levels in the lateral regions. RAR-alpha was associated with crest cell emigration and migration, while RAR-gamma was present in the primitive streak region throughout the period of neurulation. There was a change from RAR-beta to RAR-gamma expression at the junction between closed and open neural epithelium at the caudal neuropore. RAR-alpha and RAR-beta were expressed at specific levels of the hindbrain and in the spinal cord. These distribution patterns are discussed in relation to segmental expression patterns of other genes, and to maturational changes in the caudal neuropore region. The CRABP transcript distribution patterns correlated well with known target tissues of excess retinoid-induced teratogenesis (migrating primary mesenchyme and neural crest cells, preoptic hindbrain), providing further support for our hypothesis that cells expressing CRABP are those that cannot tolerate high levels of RA for their normal developmental function.

2009 ◽  
Vol 126 ◽  
pp. S106
Author(s):  
Simone Macrí ◽  
Marco Onorati ◽  
Guidalberto Manfioletti ◽  
Robert Vignali

1994 ◽  
Vol 8 (10) ◽  
pp. 699-706 ◽  
Author(s):  
Marianne Bronner‐Fraser

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Christopher J. Hindley ◽  
Alexandra Larisa Condurat ◽  
Vishal Menon ◽  
Ria Thomas ◽  
Luis M. Azmitia ◽  
...  

1992 ◽  
Vol 98 (6) ◽  
pp. S36-S41 ◽  
Author(s):  
James T Elder ◽  
Anders Åström ◽  
Ulrika Pettersson ◽  
Amir Tavakkol ◽  
Andree Krust ◽  
...  

2010 ◽  
Vol 344 (1) ◽  
pp. 500
Author(s):  
Bridget T. Jacques-Fricke ◽  
Laura S. Gammill

1998 ◽  
Vol 46 (10) ◽  
pp. 1103-1111 ◽  
Author(s):  
Marie-Pierre Gaub ◽  
Yves Lutz ◽  
Norbert B. Ghyselinck ◽  
Isabelle Scheuer ◽  
Véronique Pfister ◽  
...  

Apart from the retinoic acid nuclear receptor family, there are two low molecular weight (15 kD) cellular retinoic acid binding proteins, named CRABPI and II. Mouse monoclonal and rabbit polyclonal antibodies were raised against these proteins by using as antigens either synthetic peptides corresponding to amino acid sequences unique to CRABPI or CRABPII, or purified CRABP proteins expressed in E. coli. Antibodies specific for mouse and/or human CRABPI and CRABPII were obtained and characterized by immunocytochemistry and immunoblotting. They allowed the detection not only of CRABPI but also of CRABPII in both nuclear and cytosolic extracts from transfected COS-1 cells, mouse embryos, and various cell lines.


1983 ◽  
Vol 96 (2) ◽  
pp. 462-473 ◽  
Author(s):  
R A Rovasio ◽  
A Delouvee ◽  
K M Yamada ◽  
R Timpl ◽  
J P Thiery

Cells of the neural crest participate in a major class of cell migratory events during embryonic development. From indirect evidence, it has been suggested that fibronectin (FN) might be involved in these events. We have directly tested the role of FN in neural crest cell adhesion and migration using several in vitro model systems. Avian trunk neural crest cells adhered readily to purified plasma FN substrates and to extracellular matrices containing cellular FN. Their adhesion was inhibited by antibodies to a cell-binding fragment of FN. In contrast, these cells did not adhere to glass, type I collagen, or to bovine serum albumin in the absence of FN. Neural crest cell adhesion to laminin (LN) was significantly less than to FN; however, culturing of crest cells under conditions producing an epithelioid phenotype resulted in cells that could bind equally as well to LN as to FN. The migration of neural crest cells appeared to depend on both the substrate and the extent of cell interactions. Cells migrated substantially more rapidly on FN than on LN or type I collagen substrates; if provided a choice between stripes of FN and glass or LN, cells migrated preferentially on the FN. Migration was inhibited by antibodies against the cell-binding region of FN, and the inhibition could be reversed by a subsequent addition of exogenous FN. However, the migration on FN was random and displayed little persistence of direction unless cells were at high densities that permitted frequent contacts. The in vitro rate of migration of cells on FN-containing matrices was 50 microns/h, similar to their migration rates along the narrow regions of FN-containing extracellular matrix in migratory pathways in vivo. These results indicate that FN is important for neural crest cell adhesion and migration and that the high cell densities of neural crest cells in the transient, narrow migratory pathways found in the embryo are necessary for effective directional migration.


1996 ◽  
Vol 14 (3) ◽  
pp. 297-314 ◽  
Author(s):  
Roberto Perris ◽  
Ralph Brandenberger ◽  
Matthias Chiquet

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