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D-type cyclins and G1 progression during liver development in the rat

Joan M Boylan1, Philip A Gruppuso

  • 1Department of Pediatrics, Rhode Island Hospital and Brown University, Providence, RI 02903, USA. Joan_Boylan@brown.edu

Biochemical and Biophysical Research Communications
|April 6, 2005
PubMed

Insights

During liver development, fetal hepatocytes utilize cyclin D2/D3 complexes, switching to cyclin D1:CDK4 complexes as they mature and become dependent on mitogenic signaling.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • Cell cycle progression through G1 phase is regulated by cyclin-dependent kinases (CDKs) and cyclins.
  • Hepatocyte proliferation during late gestation liver development is partially independent of mature signaling pathways.

Purpose of the Study:

  • To identify G1-phase cyclins and CDKs active during rat liver development.
  • To investigate the role of these complexes in hepatocyte proliferation.

Main Methods:

  • RNase protection assay to quantify cyclin mRNA levels.
  • Western immunoblotting to assess protein expression and complex formation.
  • Analysis of retinoblastoma protein (Rb) phosphorylation.

Main Results:

  • Cyclin D1 levels were similar in fetal and adult liver; its partner was CDK4 post-hepatectomy.
  • Cyclins D2 and D3 predominated in fetal liver, complexed with CDK4 and CDK6.
  • Cyclins E1/E2 and Rb phosphorylation were higher in fetal liver.
  • CDK6 was minimally expressed in adult quiescent or regenerating liver.

Conclusions:

  • Liver development involves a shift from cyclin D2/D3:CDK4/6 complexes to cyclin D1:CDK4 complexes.
  • This switch may correlate with the maturation of hepatocyte dependence on mitogenic signaling.

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