title: Genes coding for cyclin-dependent kinase inhibitors are fragile in Xenopus.
abstract: Cell proliferation is strictly regulated by the dosage balance among cell-cycle regulators such as CDK/cyclin complexes and CDK-Inhibitors. Even in the allotetraploid genome of Xenopus laevis, the dosage balance must be maintained for animals to stay alive, and the duplicated homeologous genes seem to have gradually changed, through evolution, resulting in the best genes for them to thrive. In the Xenopus laevis genome, while homeologous gene pairs of CDKs are fundamentally maintained and a few cyclin genes are amplified, homeologous gene pairs of the important CDK-Inhibitors, CDKn1c and CDKn2a, are deleted from chromosomes L and S. Although losses of CDKn1c and CDKn2a can lead to diseases in humans, their loss in X. laevis does not affect the animals' health. Also, another gene coding CDKn1b is lost besides CDKn1c and CDKn2a in the genome of Xenopus tropicalis. These findings suggest a high resistance of Xenopus to diseases. We also found that CDKn2c.S expression is higher than that of CDKn2c.L, and a conserved noncoding sequence (CNS) of CDKn2c genomic loci on X. laevis chromosome S and X. tropicalis has an enhancement activity in regulating the different expression. These findings together indicate a surprising fragility of CDK inhibitor gene loci in the Xenopus genome in spite of their importance, and may suggest that factors other than CDK-inhibitors decelerate cell-cycling in Xenopus.
authors.affiliation: School of Life Science and Technology, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama 226-8501, Japan. Electronic address: ttanaka@bio.titech.ac.jp.
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Tanaka
authors.affiliation: Institute for Promotion of Medical Science Research, Yamagata University Faculty of Medicine, 2-2-2 Iida-Nishi, Yamagata, Yamagata 990-9585, Japan.
authors.forename: Haruki
authors.initials: H
authors.lastname: Ochi
authors.affiliation: Institute for Amphibian Biology, Graduate School of Science, Hiroshima University, 1-3-1 Kagamiyama, Higashi-Hiroshima, Hiroshima 739-8526, Japan.
authors.forename: Shuji
authors.initials: S
authors.lastname: Takahashi
authors.affiliation: National Institute for Basic Biology, National Institutes of Natural Sciences, 38 Nishigonaka, Myodaiji, Okazaki 444-8585, Aichi, Japan.
authors.forename: Naoto
authors.initials: N
authors.lastname: Ueno
authors.affiliation: Department of Biological Sciences, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
authors.forename: Masanori
authors.initials: M
authors.lastname: Taira
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D002453:Cell Cycle / Q000235:genetics / Q000502:physiology; D050756:Cyclin-Dependent Kinase Inhibitor Proteins / Q000235:genetics*; D018844:Cyclin-Dependent Kinases / Q000235:genetics; D004171:Diploidy; D004625:Embryo, Nonmammalian / Q000502:physiology; D019143:Evolution, Molecular; D017353:Gene Deletion; D049810:Genetic Speciation; D042822:Genomic Instability; D005810:Multigene Family; D016415:Sequence Alignment; D017386:Sequence Homology, Amino Acid; D013045:Species Specificity; D057891:Tetraploidy; D014981:Xenopus / Q000196:embryology / Q000235:genetics*; D029867:Xenopus Proteins / Q000235:genetics*; D014982:Xenopus laevis / Q000196:embryology / Q000235:genetics
chemical_list: D050756:Cyclin-Dependent Kinase Inhibitor Proteins; D029867:Xenopus Proteins; D018844:Cyclin-Dependent Kinases
keywords: CDK inhibitor; Cell cycle; Genome; Xenopus laevis