Short-period mutations of per affect a double-time-dependent step in the Drosophila circadian clock

Adrian Rothenfluh, Marla Abodeely, Michael W. Young

Research output: Contribution to journalArticle

69 Scopus citations

Abstract

Circadian (24 hour) PERIOD (PER) protein oscillation is dependent on the double-time (dbt) gene, a casein kinase lε homolog [1-3]. Without dbt activity, hypophosphorylated PER proteins over-accumulate, indicating that dbt is required for PER phosphorylation and turnover [3,4]. There is evidence of a similar role for casein kinase lε in the mammalian circadian clock [5,6]. We have isolated a new dbt allele, dbt(ar), which causes arrhythmic locomotor activity in homozygous viable adults, as well as molecular arrhythmicity, with constitutively high levels of PER proteins, and low levels of TIMELESS (TIM) proteins. Short-period mutations of per, but not of tim, restore rhythmicity to dbt(ar) flies. This suppression is accompanied by a restoration of PER protein oscillations. Our results suggest that short-period per mutations, and mutations of dbt, affect the same molecular step that controls nuclear PER turnover. We conclude that, in wild-type flies, the previously defined PER 'short domain' [7,8] may regulate the activity of DBT on PER.

Original languageEnglish (US)
Pages (from-to)1399-1402
Number of pages4
JournalCurrent Biology
Volume10
Issue number21
DOIs
StatePublished - Nov 2 2000

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)

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