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Cip/Kip cyclin-dependent protein kinase inhibitors and the road to polyploidy

Zakir Ullah1, Chrissie Y Lee, Melvin L Depamphilis

  • 1National Institute of Child Health and Human Development, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892-2753, USA. depamphm@mail.nih.gov.

Cell Division
|June 4, 2009
PubMed

Insights

Mammalian cell cycle regulators p21Cip1 and p57Kip2 are induced during trophoblast stem cell differentiation. These proteins may drive polyploidy in mammals by inhibiting cell division and DNA damage responses.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • Cyclin-dependent kinases (CDKs) regulate cell cycle progression in eukaryotes.
  • p27Kip1 inhibits premature G1 to S-phase transition.
  • p57Kip2 and p21Cip1 are mammalian CDK inhibitors with roles in differentiation.

Purpose of the Study:

  • To investigate the roles of p21Cip1 and p57Kip2 in mammalian polyploidy during development.
  • To determine if these proteins induce or maintain polyploidy in trophoblast stem cells.

Main Methods:

  • Studied expression of p57Kip2 and p21Cip1 during trophoblast stem cell differentiation.
  • Assessed the impact of p57Kip2 on CDK1 activity.
  • Examined the role of p21Cip1 in the DNA damage response pathway.

Main Results:

  • p57Kip2 expression is induced during trophoblast stem cell to trophoblast giant cell differentiation.
  • p57Kip2 inhibits CDK1 activity, leading to genome endoreduplication.
  • p21Cip1 expression is also induced and appears to suppress DNA damage response.

Conclusions:

  • p57Kip2 and p21Cip1 are key regulators of polyploidy in mammalian development.
  • These proteins likely induce and maintain polyploidy by controlling cell cycle and DNA damage pathways.

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