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Hematopoietic cells from mice deficient in wild-type p53 are more resistant
to induction of apoptosis by some agents
J Lotem and L Sachs
Department of Molecular Genetics and Virology, Weizmann Institute of
Science, Rehovot, Israel.
Wild-type p53 is a tumor-suppressor gene that can induce cell death by
apoptosis when expressed in myeloid leukemic and some other types of tumor
cells. However, the question remained as to what extent wild-type p53 is a
mediator of apoptosis in normal cells. We have used mice deficient in
wild-type p53 to determine whether induction of apoptosis in hematopoietic
cells from these p53 deficient mice is defective. We show here that bone
marrow myeloid progenitor cells from p53-deficient mice are more resistant
to induction of apoptosis when there was only a low concentration of the
viability factors granulocyte-macrophage colony-stimulating factor;
interleukins-1 alpha, -3, and -6; or stem cell factor; or when apoptosis
was induced in these cells by irradiation or heat shock. The loss of one
allele of wild-type p53 was sufficient for increased resistance. The higher
resistance to apoptosis in p53-deficient mice was also found in irradiated
thymocytes, but not in thymocytes treated with dexamethasone or in mature
peritoneal granulocytes. The degree of resistance in irradiated myeloid
progenitors and thymocytes showed a dosage effect of the number of wild-
type p53 genes. The results show that wild-type p53 is involved in the
induction of apoptosis by some agents in normal hematopoietic cells. Loss
of wild-type p53 can, therefore, contribute to tumor development by
decreasing cell death at low concentrations of viability factors and after
exposure to a DNA-damaging agent. The results also show that there are
wild-type p53-dependent and -independent pathways of normal cell apoptosis.
Volume 82,
Issue 4,
pp. 1092-1096,
08/15/1993
Copyright © 1993 by The American Society of Hematology
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