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Dev Biol 2017 Jun 15;4262:291-300. doi: 10.1016/j.ydbio.2016.06.019.
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Genes coding for cyclin-dependent kinase inhibitors are fragile in Xenopus.

Tanaka T , Ochi H , Takahashi S , Ueno N , Taira M .

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.

PubMed ID: 27393661
Article link: Dev Biol

Species referenced: Xenopus tropicalis Xenopus laevis
Genes referenced: ccnb1.2 ccndx ccnh cdk4 cdk7 cdkn1b cdkn1c cdkn2c cdknx cox7c serinc5 tmem161b

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