Loss of circadian rhythmicity in agingmPer1-/-mCry2-/-mutant mice

Jun 5, 2003Genes & development

Loss of daily biological rhythms in aging mice lacking mPer1 and mCry2 genes

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Circadian BiologyCircadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

mPer1-/- mCry2-/- mice exhibited a decay of the circadian clock with age at both behavioral and molecular levels.

  • The mPer1, mPer2, mCry1, and mCry2 genes are crucial for the function of the circadian clock in mammals.
  • In vitro studies indicate interactions among mPER and mCRY proteins.
  • Different combinations of mPer/mCry double-mutant mice reveal non-redundant roles of mPER and mCRY complexes in vivo.
  • mCry2 has been identified as a nonallelic suppressor of mPer2 within the core clock mechanism.
  • Age-related decay of the circadian clock suggests that mPER and mCRY proteins play distinct roles in regulating transcription.

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