scholarly journals Substratum-growth factor collaborations are required for the mitogenic activities of activin and FGF on embryonal carcinoma cells.

1991 ◽  
Vol 114 (4) ◽  
pp. 841-846 ◽  
Author(s):  
D Schubert ◽  
H Kimura
Keyword(s):  
Tissue Culture ◽  
Embryonal Carcinoma ◽  
Activin A ◽  
Carcinoma Cells ◽  
Matrix Proteins ◽  
P19 Cells ◽  
Embryonal Carcinoma Cells ◽  
Tissue Culture Plastic ◽  
Mitogenic Response ◽  
Serum Free

When P19 mouse embryonal carcinoma cells are grown in a serum-free N2 medium on surfaces of tissue culture plastic, they die within two days. The death of these P19 cells is prevented by activin A and basic FGF (bFGF). The cells do not divide under these conditions. However, when P19 cells are cultured on substrata of extracellular matrix proteins such as laminin and fibronectin, activin A and bFGF are potent mitogens. These data show that the substratum to which cells are exposed can regulate their mitogenic response to growth factors.

scholarly journals Induction and repression of mammalian achaete-scute homologue (MASH) gene expression during neuronal differentiation of P19 embryonal carcinoma cells

Development ◽  
1992 ◽  
Vol 114 (1) ◽  
pp. 75-87 ◽  
Author(s):  
J.E. Johnson ◽  
K. Zimmerman ◽  
T. Saito ◽  
D.J. Anderson
Keyword(s):  
Retinoic Acid ◽  
Neuronal Differentiation ◽  
Embryonal Carcinoma ◽  
Model System ◽  
Neuronal Morphology ◽  
Carcinoma Cells ◽  
P19 Cells ◽  
Embryonal Carcinoma Cells ◽  
Bhlh Genes ◽  
P19 Embryonal Carcinoma Cells

MASH1 and MASH2, mammalian homologues of the Drosophila neural determination genes achaete-scute, are members of the basic helix-loop-helix (bHLH) family of transcription factors. We show here that murine P19 embryonal carcinoma cells can be used as a model system to study the regulation and function of these genes. MASH1 and MASH2 display complementary patterns of expression during the retinoic-acid-induced neuronal differentiation of P19 cells. MASH1 mRNA is undetectable in undifferentiated P19 cells but is induced to high levels by retinoic acid coincident with neuronal differentiation. In contrast, MASH2 mRNA is expressed in undifferentiated P19 cells and is repressed by retinoic acid treatment. These complementary expression patterns suggest distinct functions for MASH1 and MASH2 in development, despite their sequence homology. In retinoic-acid-treated P19 cells, MASH1 protein expression precedes and then overlaps expression of neuronal markers. However, MASH1 is expressed by a smaller proportion of cells than expresses such markers. MASH1 immunoreactivity is not detected in differentiated cells displaying a neuronal morphology, suggesting that its expression is transient. These features of MASH1 expression are similar to those observed in vivo, and suggest that P19 cells represent a good model system in which to study the regulation of this gene. Forced expression of MASH1 was achieved in undifferentiated P19 cells by transfection of a cDNA expression construct. The transfected cells expressing exogenous MASH1 protein contained E-box-binding activity that could be super-shifted by an anti-MASH1 antibody, but exhibited no detectable phenotypic changes. Thus, unlike myogenic bHLH genes, such as MyoD, which are sufficient to induce muscle differentiation, expression of MASH1 appears insufficient to promote neurogenesis.

Transient expression of the proto-oncogene int-1 during differentiation of P19 embryonal carcinoma cells

1989 ◽  
Vol 9 (3) ◽  
pp. 1357-1361
Author(s):  
E Schuuring ◽  
L van Deemter ◽  
H Roelink ◽  
R Nusse
Keyword(s):  
Retinoic Acid ◽  
Neural Development ◽  
Time Course ◽  
Embryonal Carcinoma ◽  
Dose Dependence ◽  
Carcinoma Cells ◽  
P19 Cells ◽  
Embryonal Carcinoma Cells ◽  
P19 Embryonal Carcinoma Cells

In mouse embryos, the int-1 proto-oncogene is transiently expressed in areas of the developing neural system. Retinoic acid-treated P19 embryonal carcinoma cells have often been used as an in vitro model for the molecular basis of neural development. We shown here that int-1 is transiently expressed in differentiated P19 cells. The time course and retinoic acid dose dependence of int-1 expression suggest that the gene is specifically expressed during early neural differentiation. P19 cells may be a useful model to assist in the study, at the cellular level, of the role of int-1 in neural development.

Analysis of the Response of Human Embryonal Carcinoma Cells to Activin A

1997 ◽  
pp. 308-311 ◽  
Author(s):  
Andrea Caricasole ◽  
Ron H. N. Van Schaik ◽  
Laura M. Zeinstra ◽  
Cristel D. J. Wierikx ◽  
Leendert L. H. J. Looijenga ◽  
...  
Keyword(s):  
Embryonal Carcinoma ◽  
Activin A ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells

Effects of taxol on the polymerization and posttranslational modification of class III β-tubulin in P19 embryonal carcinoma cells

1995 ◽  
Vol 73 (9-10) ◽  
pp. 687-694 ◽  
Author(s):  
Nicole B. Laferrière ◽  
D. L. Brown
Keyword(s):  
Neurite Outgrowth ◽  
Posttranslational Modification ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Specific Class ◽  
P19 Cells ◽  
Embryonal Carcinoma Cells ◽  
Class Iii ◽  
P19 Embryonal Carcinoma Cells ◽  
Β Tubulin

Undifferentiated P19 embryonal carcinoma cells and P19 cells induced to differentiate along a neuronal pathway by 10−6 M retinoic acid were treated with taxol to examine the effects of this microtubule-stabilizing drug on the subcellular sorting of class III β-tubulin and on neurite outgrowth. P19 cells were grown on cover slips and then treated with taxol at concentrations of 10−6 to 10−9 M for 24 h. The microtubule cytoskeleton was examined after double-immunofluorescence labelling with a monoclonal antibody to α-tubulin (YOL 1/34) and a monoclonal neuron-specific class III β-tubulin antibody (TuJ1). Treatment of undifferentiated P19 cells with concentrations of taxol greater than 4 × 10−8 M caused microtubule bundling and multiple aster formation and promoted polymerization of the low levels of class III β-tubulin found in these cells. In neurons, at 2 × 10−8 M taxol, bundling of microtubules at the base of the neurite was apparent. At taxol concentrations greater than 1 × 10−7 M, enhanced assembly of class III β-tubulin was apparent, although long neurites were not observed. Using isoelectric focusing followed by western blotting, we detected an additional isoform of class III β-tubulin after treatment with 10−6 M taxol. These results indicate taxol treatment alters the normal subcellular sorting of tubulin isotypes, promotes the polymerization and posttranslational modification of class III β-tubulin, and interferes with neurite outgrowth.Key words: tubulin, taxol, microtubule, posttranslational modification, neurite outgrowth.

scholarly journals Retinoic acid-induced neural differentiation of embryonal carcinoma cells.

1983 ◽  
Vol 3 (12) ◽  
pp. 2271-2279 ◽  
Author(s):  
E M Jones-Villeneuve ◽  
M A Rudnicki ◽  
J F Harris ◽  
M W McBurney
Keyword(s):  
Retinoic Acid ◽  
Embryonal Carcinoma ◽  
Neuronal Cell ◽  
Carcinoma Cells ◽  
Polyamine Metabolism ◽  
P19 Cells ◽  
Embryonal Carcinoma Cells ◽  
Acetyl Cholinesterase ◽  
Choline Acetyl Transferase ◽  
Cholinesterase Activities

We have previously shown that the P19 line of embryonal carcinoma cells develops into neurons, astroglia, and fibroblasts after aggregation and exposure to retinoic acid. The neurons were initially identified by their morphology and by the presence of neurofilaments within their cytoplasm. We have more fully documented the neuronal nature of these cells by showing that their cell surfaces display tetanus toxin receptors, a neuronal cell marker, and that choline acetyl-transferase and acetyl cholinesterase activities appear coordinately in neuron-containing cultures. Several days before the appearance of neurons, there is a marked decrease in the amount of an embryonal carcinoma surface antigen, and at the same time there is a substantial decrease in the volumes of individual cells. Various retinoids were able to induce the development of neurons in cultures of aggregated P19 cells, but it did not appear that polyamine metabolism was involved in the effect. We have isolated a mutant clone which does not differentiate in the presence of any of the drugs which are normally effective in inducing differentiation of P19 cells. This mutant and others may help to elucidate the chain of events triggered by retinoic acid and other differentiation-inducing drugs.

Cellular aggregation enhances MyoD-directed skeletal myogenesis in embryonal carcinoma cells

1994 ◽  
Vol 14 (12) ◽  
pp. 8451-8459
Author(s):  
I S Skerjanc ◽  
R S Slack ◽  
M W McBurney
Keyword(s):  
Skeletal Muscle ◽  
Embryonal Carcinoma ◽  
Cell Aggregation ◽  
Carcinoma Cells ◽  
P19 Cells ◽  
Embryonal Carcinoma Cells ◽  
Transfected Cells ◽  
Primary Myoblasts ◽  
Cellular Aggregation ◽  
Genes Encoding

When introduced into P19 embryonal carcinoma cells, recombinant genes encoding MyoD converted only a small percentage (< 3%) of the transfected cells into skeletal muscle. We isolated stably transfected cells that expressed the MyoD transcript. These P19[MyoD] cells continued to express markers characteristic of undifferentiated stem cells but also expressed myf-5 and the myotonic dystrophy kinase, transcripts normally present in myoblasts but absent from P19 cells. Aggregation of P19[MyoD] cells induced the expression of myogenin, desmin, and the retinoblastoma protein and resulted in the rapid and abundant development of skeletal muscle. Both the embryonic and the slow isoforms of myosin heavy chain were present in this muscle, indicating that it resembled skeletal muscle formed from primary myoblasts. Since aggregation of P19 cells normally results in inefficient differentiation and the development of only low levels of cardiac muscle but no skeletal muscle, we conclude that MyoD imposes the skeletal muscle program on P19 cells and that the differentiation of these cells requires inductive events provided by cell aggregation.

Retinoic acid-induced neural differentiation of embryonal carcinoma cells

1983 ◽  
Vol 3 (12) ◽  
pp. 2271-2279
Author(s):  
E M Jones-Villeneuve ◽  
M A Rudnicki ◽  
J F Harris ◽  
M W McBurney
Keyword(s):  
Retinoic Acid ◽  
Embryonal Carcinoma ◽  
Neuronal Cell ◽  
Carcinoma Cells ◽  
Polyamine Metabolism ◽  
P19 Cells ◽  
Embryonal Carcinoma Cells ◽  
Acetyl Cholinesterase ◽  
Choline Acetyl Transferase ◽  
Cholinesterase Activities

We have previously shown that the P19 line of embryonal carcinoma cells develops into neurons, astroglia, and fibroblasts after aggregation and exposure to retinoic acid. The neurons were initially identified by their morphology and by the presence of neurofilaments within their cytoplasm. We have more fully documented the neuronal nature of these cells by showing that their cell surfaces display tetanus toxin receptors, a neuronal cell marker, and that choline acetyl-transferase and acetyl cholinesterase activities appear coordinately in neuron-containing cultures. Several days before the appearance of neurons, there is a marked decrease in the amount of an embryonal carcinoma surface antigen, and at the same time there is a substantial decrease in the volumes of individual cells. Various retinoids were able to induce the development of neurons in cultures of aggregated P19 cells, but it did not appear that polyamine metabolism was involved in the effect. We have isolated a mutant clone which does not differentiate in the presence of any of the drugs which are normally effective in inducing differentiation of P19 cells. This mutant and others may help to elucidate the chain of events triggered by retinoic acid and other differentiation-inducing drugs.

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