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Mammalian cryptochromes impinge on cell cycle progression in a circadian clock-independent manner

Eugin Destici1, Małgorzata Oklejewicz, Shoko Saito

  • 1Department of Genetics, Erasmus University Medical Center, Rotterdam, The Netherlands.

Cell Cycle (Georgetown, Tex.)
|October 29, 2011
PubMed

Insights

The circadian clock

Area of Science:

  • Cell Biology
  • Chronobiology
  • Genetics

Background:

  • The intracellular circadian clock regulates cell cycle progression, potentially minimizing DNA damage in replicating cells.
  • Defects in core clock genes disrupt circadian rhythmicity, affecting genotoxic stress response and proliferation in vivo.
  • The extent to which these phenotypes are cell-autonomous versus systemically controlled remains unclear.

Purpose of the Study:

  • To investigate the cell-autonomous DNA damage sensitivity and proliferative capacity of primary fibroblasts lacking CRY proteins (Cry1-/-|Cry2-/-).
  • To determine if circadian clock-independent mechanisms underlie CRY protein's influence on cell cycle progression.

Main Methods:

  • Cultured primary wild-type, Cry1-/-|Cry2-/-, Cry1+/-|Cry2-/-, and Cry1-/-|Cry2+/- fibroblasts were used.
  • Cells were exposed to genotoxic agents in vitro to assess DNA damage response and proliferation rates.
  • Gene expression analysis focused on Bmal1-dependent pathways.

Main Results:

  • Absence of CRY proteins did not alter cell-autonomous DNA damage response in vitro.
  • Cry-deficient fibroblasts exhibited faster proliferation rates compared to wild-type.
  • Accelerated cell cycle progression in Cry-deficient cells was linked to dysregulated Bmal1-dependent gene expression.

Conclusions:

  • CRY proteins influence cell cycle progression in a cell-autonomous, circadian clock-independent manner.
  • Faster proliferation in Cry-deficient cells is mediated by Bmal1 pathway dysregulation.
  • Discrepancies between in vivo and in vitro findings may stem from systemic circadian control, not solely cell-autonomous effects.

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