IL3-dependent cells die by apoptosis on removal of their growth factor.
The IL3-dependent cell line FDCP-2 dies within 32 h of removal of IL3. Electron microscope studies indicate that 22 h after IL3 removal the nuclei are condensed, but the morphology of mitochondria and ribosomes is preserved. This pattern is characteristic of apoptosis. IL3 removal also results in the fragmentation of DNA into nucleosome-sized pieces, suggesting that an endonuclease is activated. The protein synthesis inhibitor, cycloheximide, enhances survival on IL3 removal, suggesting that death is an active process. The nuclease inhibitor, aurintricarboxylic acid, also enhances survival, suggesting a causal role for DNA fragmentation in apoptosis.
Crompton
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ICRF Tumour Immunology Unit, Biology Department, University College London.
D000818:Animals; D001312:Aurintricarboxylic Acid / Q000633:toxicity; D002460:Cell Line / Q000648:ultrastructure; D002470:Cell Survival / Q000187:drug effects* / Q000235:genetics; D003513:Cycloheximide / Q000633:toxicity; D004249:DNA Damage; D007377:Interleukin-3 / Q000502:physiology*; D051379:Mice
D007377:Interleukin-3; D001312:Aurintricarboxylic Acid; D003513:Cycloheximide