New short period mutations of the Drosophila clock gene per

Neuron. 1992 Sep;9(3):575-81. doi: 10.1016/0896-6273(92)90194-i.

Abstract

Earlier work has indicated that the period length of Drosophila circadian behavioral rhythms is dependent on the abundance of the period (per) gene product. Increased expression of this gene has been associated with period shortening for both the circadian eclosion (pupal hatching) rhythm and circadian locomotor activity rhythms of adult Drosophila. In this study it is shown that a wide variety of missense mutations, affecting a region of the per protein consisting of approximately 20 aa, predominantly generate short period phenotypes. The prevalence of such mutations suggests that short period phenotypes may result from loss or depression of function in this domain of the per protein. Possibly mutations in the region eliminate a regulatory function provided by this segment, or substantially increase stability of the mutant protein.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Animals, Genetically Modified
  • Base Sequence
  • Biological Clocks / physiology*
  • Chromosome Mapping
  • Drosophila / genetics*
  • Drosophila Proteins
  • Genes*
  • Molecular Sequence Data
  • Mutation*
  • Nuclear Proteins*
  • Oligonucleotide Probes / genetics
  • Period Circadian Proteins
  • Proteins / chemistry
  • Proteins / genetics*
  • Proteins / metabolism

Substances

  • Drosophila Proteins
  • Nuclear Proteins
  • Oligonucleotide Probes
  • PER protein, Drosophila
  • Period Circadian Proteins
  • Proteins