A Transfected c-myc Oncogene Inhibits Mouse Erythroleukemic Differentiation
Cellular differentiation is a complex process for which the molecular mechanisms are poorly understood. One useful model for the study of differentiation is the Friend virus derived (Friend 1971) mouse erythroleukemia (MEL) cell lines. These transformed early erythroid precursors can be induced to terminally differentiate into mature erythroid cells by a variety of seemingly unrelated agents including dimethyl, sulfoxide (DMSO) (Marks 1978). Following DMSO induction, the majority of cells become irreversibly committed to differentiation, undergoing several rounds of cell division before ceasing to replicate (Gusella 1976; Fibach 1977). These terminally differentiated cells express high levels of hemoglobin (Boyer 1972; Ostertag 1972). After DMSO induction of MEL cells there is a biphasic decline in steady state levels of c-myc (Lachman 1984; Kirsch 1985) and c-myb mRNAs (Kirsch 1985). We sought to determine if the down regulation of c-myc mRNA is a necessary step for DMSO induced differentiation. Our experiments indicate that expression of a transfected human c-myc gene inhibits the terminal differentiation of MEL cells.
KeywordsErythroid Differentiation Neomycin Resistance Gene Friend Virus Mouse Erythroleukemia Biphasic Decline
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