[Damage to the genome, p53 and cell polyploidization in ontogeny].
The protein p53 is a universal tumor suppressor in humans and negative regulator of cell proliferation, which is induced in cells in response to the damage of DNA and controls arrest of the cell cycle at specific checkpoints. A recently discovered function of gene p53 is the maintenance of the diploid state of the genome and a block of the formation of the population of cycling polyploids. This review examines models of disturbed control of the cell cycle due to loss, inactivation, or hyperexpression of gene p53 or its effector gene p21 in transgenic animals, i.e., homozygous mutant mice (p53-/-), (ERCC-1-/-), as well as in genetically defective cell lines in vitro. We discuss mechanisms responsible for the transition from the diploid to the polyploid state owing to the disturbed control of cell cycle by p53 and arising during the ontogenetic polyploidization of cells in normal animals.
Uryvaeva
I V
IV
Kol'tsov Institute of Developmental Biology, Russian Academy of Sciences, Moscow, Russia.
D000818:Animals; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000235:genetics; D004249:DNA Damage / Q000235:genetics*; D005786:Gene Expression Regulation / Q000235:genetics; D016678:Genome; D051379:Mice; D008817:Mice, Mutant Strains; D008822:Mice, Transgenic; D011123:Polyploidy; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
C493957:Cdkn1a protein, mouse; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D016159:Tumor Suppressor Protein p53
Povrezhdenie genoma, p53 i poliploidizatsiia kletok v ontogeneze.