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Analysis of Cell Cycle Position in Mammalian Cells
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RB, p130 and p107 differentially repress G1/S and G2/M genes after p53 activation

Amy E Schade1,2, Martin Fischer2,3, James A DeCaprio1,2,4

  • 1Program in Virology, Division of Medical Sciences, Graduate School of Arts and Sciences, Harvard University, Boston, MA 02115, USA.

Nucleic Acids Research
|November 1, 2019
PubMed

Insights

DNA damage triggers p53 activation, leading to differential repression of cell cycle genes. RB, p130, and p107 proteins play specific roles in regulating G1/S and G2/M gene expression and cell cycle progression.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Cell cycle gene expression is tightly regulated in two waves: G1/S for DNA synthesis and G2/M for mitosis.
  • The Retinoblastoma protein (RB) and DREAM complex (DP, RB-like, E2F4, and MuvB) normally repress cell cycle genes during G1.
  • DNA damage activates p53, increasing p21 levels and inhibiting cell cycle progression.

Purpose of the Study:

  • To investigate the differential repression of G1/S and G2/M genes by RB and RB-like proteins (p130, p107) in response to DNA damage.
  • To elucidate the specific roles of RB, p130-DREAM, and p107-DREAM in p53/p21-mediated cell cycle gene repression.

Main Methods:

  • Gene expression profiling of primary human fibroblasts after inducing DNA damage.
  • Assessment of the effects of DNA damage on G1/S and G2/M gene expression.
  • Analysis of the roles of RB, p130, and p107 in gene repression pathways.

Main Results:

  • Upon p53 activation, p130 and RB cooperated to repress G1/S genes.
  • p107 contributed to G1/S gene repression in the absence of RB and p130.
  • p130 and p107 repressed G2/M genes following p53 activation, leading to reduced entry into mitosis.

Conclusions:

  • RB, p130-DREAM, and p107-DREAM exhibit distinct roles in the p53 and p21-mediated repression of cell cycle genes.
  • The study reveals specific mechanisms by which DNA damage signaling impacts cell cycle control through differential gene repression.

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