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Expression of c-myc and macromolecular synthesis have been associated with physiological cell death. We have studied their requirement for the death of factor (interleukin-3)-dependent cells (FDC-P1) bearing an inducible bcl-2 expression construct. FDC-P1 cells expressing bcl-2 turned off expression of c-myc when deprived of interleukin-3 but remained viable as long as bcl-2 was maintained. A subsequent decline in Bcl-2 allowed the cells to undergo apoptosis directly from G0, in the absence of detectable c-myc expression. Thus c-myc expression may lead to apoptosis in some cases but is not directly involved in the mechanism of physiological cell death that can be controlled by Bcl-2. The macromolecular synthesis inhibitors actinomycin D and cycloheximide triggered rapid cell death of FDC-P1 cells in the presence of interleukin-3, but the cells could be protected by Bcl-2. Thus, the cell death machinery can exist in a quiescent state and can be activated by mechanisms that do not require synthesis of RNA or protein.

Type

Journal article

Journal

Mol Cell Biol

Publication Date

11/1993

Volume

13

Pages

7000 - 7005

Keywords

Animals, Apoptosis, Blotting, Northern, Cell Death, Cell Line, Cycloheximide, Dactinomycin, Gene Expression, Genes, myc, Hematopoietic Stem Cells, Humans, Kinetics, Poly A, Protein-Tyrosine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcl-2, Proto-Oncogene Proteins c-myc, Proto-Oncogenes, RNA, RNA, Messenger, Resting Phase, Cell Cycle, Transfection