Evidence that Shh cooperates with a retinoic acid inducible co-factor to establish ZPA-like activity

Development ◽  
1996 ◽  
Vol 122 (2) ◽  
pp. 537-542 ◽  
Author(s):  
T. Ogura ◽  
I.S. Alvarez ◽  
A. Vogel ◽  
C. Rodriguez ◽  
R.M. Evans ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Sonic Hedgehog ◽  
Embryonal Carcinoma ◽  
Carcinoma Cell ◽  
Retinoic Acid Receptor ◽  
Mirror Image ◽  
Limb Bud ◽  
Embryonal Carcinoma Cell ◽  
Embryonal Carcinoma Cell Line ◽  
Vertebrate Limb

Patterning across the anteroposterior axis of the vertebrate limb bud involves a signal from the polarizing region, a small group of cells at the posterior margin of the bud. Retinoic acid (RA; Tickle, C., Alberts, B., Wolpert, L. and Lee, J. (1982) Nature 296, 554–566) and Sonic hedgehog (Shh; Riddle, R. D. Johnson, R. L., Laufer, E. and Tabin, C. J. (1993) Cell 25, 1401–1416; Chang, D. T., Lopez, A., von Kessler, D. P., Chiang, C., Simandl, B. K., Zhao, R., Seldin, M. F., Fallon, J. F. and Beachy, P. A. (1994 Development 120, 3339–3353) have been independently postulated as such signals because they can mimic the mirror image digit duplication obtained after grafting polarizing cells to the anterior of limb buds. Here we show that a embryonal carcinoma cell line, P19, transfected with a Shh expression vector shows low polarizing activity, but when cultured with retinoic acid, duplications like those induced by the polarizing region (ZPA) arise. Complete duplications are also obtained by cotransfecting P19 Shh cells with a constitutively active human retinoic acid receptor (VP16-hRARalpha). These data suggest that Shh and RA cooperate in generating ZPA activity and that Shh, while essential, may not act alone in this process.

scholarly journals States of developmental commitment of a mouse embryonal carcinoma cell line differentiating along a neural pathway.

1989 ◽  
Vol 109 (5) ◽  
pp. 2481-2493 ◽  
Author(s):  
E Lang ◽  
M L Mazauric-Stüker ◽  
A Maelicke
Keyword(s):  
Retinoic Acid ◽  
Cell Line ◽  
Embryonal Carcinoma ◽  
Carcinoma Cell ◽  
Neuronal Cell ◽  
Carcinoma Cell Line ◽  
Mammalian Brain ◽  
Embryonal Carcinoma Cell ◽  
Induced Differentiation ◽  
Embryonal Carcinoma Cell Line

The embryonal carcinoma cell line PCC7-S-AzaR1 (clone 1009) has been shown to differentiate in the presence of all-trans retinoic acid and dibutyryl cAMP into cells of predominantly neural properties (Paulin, D., H. Jakob, F. Jacob, K. Weber, and M. Osborn. 1982. Differentiation. 22:90-99). By analyzing the marker expression of derivatives in further detail, we characterized the two major cell phenotypes as neuron- and fibroblast-like and the two minor ones as astroglia- and endothelial-like. The stability of developmental commitment of clone 1009 was tested by recloning. The isolated subclones exhibited different patterns of chemically induced derivatives, with some of them (denoted N-clones) producing only a single (neuronal) cell type. As shown by long-term cultures in the absence of retinoic acid, the properties of isolated subclones remained essentially stable. In contrast to the clones producing neuron-like and other derivatives upon induced differentiation, the (exclusively neuronal) derivatives of N-clones detached and died within a few days in culture. If maintained in the presence of other neural cell types, however, their survival was dramatically extended indicating a requirement for specific interactions with other cells of the same tissue. The patterns of derivatives obtained from N-clones depended on the chemical nature of the substrate on which they were grown. Thus, when seeded on laminin-coated surfaces before induced differentiation, N-clones developed not only to neuron-like derivatives but rather to the same four derivatives observed with the original cell pool. These and further results suggest a common cell lineage of the identified phenotypes. The isolated subclones of uninduced cells probably represent different states of commitment within the same developmental pathway. Their stability offers the opportunity to analyze the nature of cellular commitment on the cellular, molecular, and genetic levels. This makes the family of clones derived from PCC7-S-AzaR1 (clone 1009) cells an advantageous in vitro model of mammalian brain early ontogenesis.

scholarly journals Expression of retinoic acid nuclear receptors in the mouse embryonal carcinoma cell line PCC7-Mz1

FEBS Letters ◽  
1992 ◽  
Vol 312 (1) ◽  
pp. 75-79 ◽  
Author(s):  
Reinhard Heiermann ◽  
Martin Rentrop ◽  
Elke Lang ◽  
Alfred Maelicke
Keyword(s):  
Retinoic Acid ◽  
Cell Line ◽  
Nuclear Receptors ◽  
Embryonal Carcinoma ◽  
Carcinoma Cell ◽  
Carcinoma Cell Line ◽  
Embryonal Carcinoma Cell ◽  
Embryonal Carcinoma Cell Line

scholarly journals Distinct retinoid X receptor-retinoic acid receptor heterodimers are differentially involved in the control of expression of retinoid target genes in F9 embryonal carcinoma cells.

1997 ◽  
Vol 17 (6) ◽  
pp. 3013-3020 ◽  
Author(s):  
H Chiba ◽  
J Clifford ◽  
D Metzger ◽  
P Chambon
Keyword(s):  
Retinoic Acid ◽  
Embryonal Carcinoma ◽  
Target Genes ◽  
Retinoic Acid Receptor ◽  
Retinoid X Receptor ◽  
Embryonal Carcinoma Cell ◽  
Retinoid Receptor ◽  
Embryonal Carcinoma Cell Line ◽  
Control Of Expression

The F9 murine embryonal carcinoma cell line represents a well-established system for the study of retinoid signaling in vivo. We have investigated the functional specificity of different retinoid X receptor (RXR)-retinoic acid (RA) receptor (RAR) isotype pairs for the control of expression of endogenous RA-responsive genes, by using wild-type (WT), RXR alpha(-/-), RAR alpha(-/-), RAR gamma(-/-), RXR alpha(-/-)-RAR alpha(-/-), and RXR alpha(-/-)-RAR gamma(-/-) F9 cells, as well as panRXR and RAR isotype (alpha, beta, and gamma)-selective retinoids. We show that in these cells the control of expression of different sets of RA-responsive genes is preferentially mediated by distinct RXR-RAR isotype combinations. Our data support the conclusion that RXR-RAR heterodimers are the functional units transducing the retinoid signal and indicate in addition that these heterodimers exert both specific and redundant functions on the expression of particular sets of RA-responsive genes. We also show that the presence of a given receptor isotype can hinder the activity of another isotype and therefore that functional redundancy between retinoid receptor isotypes can be artifactually generated by gene knockouts.

Retinoic acid resistance of the variant embryonal carcinoma cell line RAC65 is caused by expression of a truncated RARα

1992 ◽  
Vol 49 (1) ◽  
pp. 27-37 ◽  
Author(s):  
Frank A.E. Kruyt ◽  
Linda J. van der Veer ◽  
Silvie Mader ◽  
Christina E. van den Brink ◽  
Alie Feijen ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Cell Line ◽  
Embryonal Carcinoma ◽  
Carcinoma Cell ◽  
Acid Resistance ◽  
Carcinoma Cell Line ◽  
Embryonal Carcinoma Cell ◽  
Embryonal Carcinoma Cell Line ◽  
Retinoic Acid Resistance
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