tim(rit) Lengthens circadian period in a temperature-dependent manner through suppression of PERIOD protein cycling and nuclear localization

Akira Matsumoto, Kenji Tomioka, Yoshihiko Chiba, Teiichi Tanimura

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

A fundamental feature of circadian clocks is temperature compensation of period. The free-running period of ritsu (tim(rit)) (a novel allele of timeless [tim]) mutants is drastically lengthened in a temperature-dependent manner. PER and TIM protein levels become lower in tim(rit) mutants as temperature becomes higher. This mutation reduces per mRNA but not tim mRNA abundance. PER constitutively driven by the rhodopsin1 promoter is lowered in rit mutants, indicating that tim(rit) mainly affects the per feedback loop at a posttranscriptional level. An excess of per+ gene dosage can ameliorate all rit phenotypes, including the weak nuclear localization of PER, suggesting that tim(rit) affects circadian rhythms by reducing PER abundance and its subsequent transportation into nuclei as temperature increases.

Original languageEnglish
Pages (from-to)4343-4354
Number of pages12
JournalMolecular and Cellular Biology
Volume19
Issue number6
Publication statusPublished - Jun 1999
Externally publishedYes

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Nuclear Proteins
Temperature
Messenger RNA
Circadian Clocks
Gene Dosage
Circadian Rhythm
Alleles
Phenotype
Mutation
Proteins

ASJC Scopus subject areas

  • Cell Biology
  • Genetics
  • Molecular Biology

Cite this

tim(rit) Lengthens circadian period in a temperature-dependent manner through suppression of PERIOD protein cycling and nuclear localization. / Matsumoto, Akira; Tomioka, Kenji; Chiba, Yoshihiko; Tanimura, Teiichi.

In: Molecular and Cellular Biology, Vol. 19, No. 6, 06.1999, p. 4343-4354.

Research output: Contribution to journalArticle

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