title: timrit Lengthens circadian period in a temperature-dependent manner through suppression of PERIOD protein cycling and nuclear localization.
abstract: A fundamental feature of circadian clocks is temperature compensation of period. The free-running period of ritsu (timrit) (a novel allele of timeless [tim]) mutants is drastically lengthened in a temperature-dependent manner. PER and TIM protein levels become lower in timrit 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 timrit 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 timrit affects circadian rhythms by reducing PER abundance and its subsequent transportation into nuclei as temperature increases.
mesh_terms: D000818:Animals; D002467:Cell Nucleus / Q000378:metabolism*; D002940:Circadian Rhythm / Q000235:genetics*; D004330:Drosophila / Q000502:physiology; D029721:Drosophila Proteins; D018628:Gene Dosage; D005816:Genetic Complementation Test; D006653:Histology; D015151:Immunoblotting; D019476:Insect Proteins; D008957:Models, Genetic; D009687:Nuclear Proteins / Q000032:analysis / Q000502:physiology*; D056950:Period Circadian Proteins; D010641:Phenotype; D017354:Point Mutation; D011995:Recombination, Genetic; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012260:Ribonucleases / Q000378:metabolism; D017422:Sequence Analysis, DNA; D013696:Temperature; D013997:Time Factors