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Phenotypic rescue of a peripheral clock genetic defect via SCN hierarchical dominance

Matthew P Pando1, David Morse, Nicolas Cermakian

  • 1Institute de Génétique et de Biologie Moléculaire et Cellulaire, CNRS-INSERM-ULP, 1 rue Laurent Fries, 67404 Illkirch, Strasbourg, France.

Cell
|August 2, 2002
PubMed

Insights

The central circadian clock (SCN) can correct genetic defects in peripheral clocks. However, it cannot restore rhythmicity to tissues lacking a functional clock.

Area of Science:

  • Chronobiology
  • Molecular Biology
  • Genetics

Background:

  • Mammalian circadian system involves central (SCN) and peripheral oscillators.
  • Communication pathways between these oscillators are not fully understood.

Purpose of the Study:

  • Investigate the influence of the central circadian clock on peripheral oscillators.
  • Determine if the SCN can compensate for genetic defects in peripheral clocks.

Main Methods:

  • Studied rhythmic behavior of mouse embryo fibroblasts (MEFs) from different genotypes.
  • Surgically implanted MEFs into host mice to assess their rhythmic characteristics in vivo.
  • Compared rhythmic properties of MEFs in culture versus within the host animal.

Main Results:

  • Per1(-/-) MEFs, with short intrinsic periods in culture, adopted host rhythms after implantation.
  • Arrhythmic clock(c/c) MEFs remained arrhythmic when implanted, regardless of host rhythmicity.
  • SCN demonstrated hierarchical dominance, compensating for genetic defects in peripheral oscillators.

Conclusions:

  • The suprachiasmatic nucleus (SCN) can override and correct intrinsic period defects in peripheral clocks.
  • A functional intrinsic clock mechanism is essential for peripheral tissues to exhibit rhythmicity, even under SCN influence.

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