Spontaneous and ionizing radiation-induced chromosomal abnormalities in p53-deficient mice.
Chromosomal abnormalities have been assessed in p53-deficient mice. The in vivo frequency of spontaneous stable aberrations in bone marrow cells was elevated by approximately 20-fold in p53 nulls and 13-fold in p53 heterozygotes compared to wild-type. No excessive induction of stable aberrations by gamma-irradiation was observed, but p53 deficiency resulted in excess radiation-induced hyperploidy (> 10-fold wild-type frequency). No influence of p53 genotype on sister chromatid exchange or G2 chromatid damage was observed in mitogen-stimulated spleen cell cultures; however, a p53 effect on postirradiation mitotic entry was seen. Abnormalities in chromosome segregation and mitotic delay following irradiation in p53-deficient mice suggest a G2-M checkpoint role for p53 and are broadly consistent with data on tumorigenesis in these animals.
Bouffler
S D
SD
Biomedical Effects Department, National Radiological Protection Board, Didcot, Oxon, United Kingdom.
Kemp
C J
CJ
Balmain
A
A
Cox
R
R
D000782:Aneuploidy; D000818:Animals; D001853:Bone Marrow / Q000528:radiation effects; D002842:Chromatids / Q000528:radiation effects; D002869:Chromosome Aberrations / Q000235:genetics*; D016158:Genes, p53 / Q000235:genetics*; D005838:Genotype; D007621:Karyotyping; D051379:Mice; D011839:Radiation, Ionizing; D012854:Sister Chromatid Exchange