The v-myc oncogene is sufficient to induce growth transformation of chick neuroretina cells.
A number of studies have shown that full transformation of non-established rodent fibroblasts can be efficiently achieved in vitro by the concerted action of two oncogenes belonging to different complementation groups. Extension of the two-genes carcinogenesis model to other differentiated cell types, presumably endowed with different controls of growth, is desirable for a better understanding of questions such as the host cell selectivity of oncogene action. A recent report claimed that cooperation between two oncogenes, v-myc and v-mil, is required to achieve transformation of chicken embryo neuroretina cells, which are characterized by a limited growth capacity in monolayer culture. Here we present evidence that the v-myc oncogene alone is sufficient to induce growth transformation of glial and neuronal precursor cell types from chick neuroretina. We also report that induction of transformation by v-myc is accompanied by faithful preservation of some of the differentiated functions of the chick cells.
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism; D001692:Biological Transport; D002448:Cell Adhesion; D002453:Cell Cycle; D002472:Cell Transformation, Viral; D002478:Cells, Cultured; D002642:Chick Embryo; D004247:DNA / Q000096:biosynthesis; D009457:Neuroglia / Q000166:cytology; D009474:Neurons / Q000166:cytology; D009856:Oncogene Proteins, Viral / Q000235:genetics; D009857:Oncogenes; D012160:Retina / Q000166:cytology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D009856:Oncogene Proteins, Viral; D001224:Aspartic Acid; D005680:gamma-Aminobutyric Acid; D004247:DNA