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High-frequency developmental abnormalities in p53-deficient mice

J F Armstrong1, M H Kaufman, D J Harrison

  • 1Department of Pathology, University Medical School, Edinburgh, UK.

Current Biology : CB
|August 1, 1995
PubMed
Summary
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Mice lacking the tumor suppressor gene p53 (p53-/-) exhibit developmental abnormalities, particularly neural tube defects in female embryos. These findings highlight p53

Area of Science:

  • Developmental Biology
  • Genetics
  • Cancer Biology

Background:

  • Null mutations in the tumor suppressor gene p53 have been generated in mice.
  • Previous studies indicated homozygous p53-null mice develop normally to birth, then rapidly succumb to neoplasia.

Purpose of the Study:

  • To investigate developmental abnormalities in p53-deficient mice.
  • To characterize the spectrum of defects and their association with p53 deficiency.

Main Methods:

  • Analysis of p53-/- embryos from p53+/- x p53+/- matings.
  • In utero analysis of p53+/- progeny from p53-/- x p53+/+ matings.
  • Assessment of progeny abnormalities following paternal irradiation prior to mating in p53-deficient backgrounds.

Main Results:

Related Experiment Videos

  • A significant proportion of female p53-/- mice die during embryogenesis or between birth and weaning due to developmental abnormalities.
  • Neural tube closure failure (exencephaly/anencephaly) occurred in 23% of p53-/- female embryos, with one affected male observed.
  • Craniofacial malformations, ocular abnormalities, and tooth formation defects were noted; irradiated males with p53 deficiency showed increased progeny abnormalities.

Conclusions:

  • p53 deficiency is associated with a high rate of developmental abnormalities, predominantly affecting neural tube closure in a female-biased manner.
  • These defects may result from a critical role of p53 during neural tube closure or increased mutation rates in p53-null gametes.