The tim Mutant of the Drosophila Rhythm Gene timeless Manifests Allele-Specific Interactions with period Gene Mutants

Rutila, Joan E.; Zeng, Hongkui; Le, Myai; Curtin, Kathryn D.; Hall, Jeffrey C.; Rosbash, Michael

doi:10.1016/s0896-6273(00)80223-8

Cited by 96 publications

(59 citation statements)

References 30 publications

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“…Therefore, it is possible that levels of GI could also be modulated by temperature. This is consistent with the temperature compensation mechanisms of other organisms (Rutila et al, 1996;Liu et al, 1997;Lahiri et al, 2005). By altering the transcription parameters of GI and LHY alone, the period of the model clock system was balanced and there was little difference in the phase of either LHY or TOC1 mRNA with temperature (see Supplemental Figure 5 online).…”

Section: Discussionsupporting

confidence: 81%

The Molecular Basis of Temperature Compensation in the Arabidopsis Circadian Clock

et al. 2006

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Circadian clocks maintain robust and accurate timing over a broad range of physiological temperatures, a characteristic termed temperature compensation. In Arabidopsis thaliana, ambient temperature affects the rhythmic accumulation of transcripts encoding the clock components TIMING OF CAB EXPRESSION1 (TOC1), GIGANTEA (GI), and the partially redundant genes CIRCADIAN CLOCK ASSOCIATED1 (CCA1) and LATE ELONGATED HYPOCOTYL (LHY). The amplitude and peak levels increase for TOC1 and GI RNA rhythms as the temperature increases (from 17 to 278C), whereas they decrease for LHY. However, as temperatures decrease (from 17 to 128C), CCA1 and LHY RNA rhythms increase in amplitude and peak expression level. At 278C, a dynamic balance between GI and LHY allows temperature compensation in wild-type plants, but circadian function is impaired in lhy and gi mutant plants. However, at 128C, CCA1 has more effect on the buffering mechanism than LHY, as the cca1 and gi mutations impair circadian rhythms more than lhy at the lower temperature. At 178C, GI is apparently dispensable for free-running circadian rhythms, although partial GI function can affect circadian period. Numerical simulations using the interlocking-loop model show that balancing LHY/CCA1 function against GI and other evening-expressed genes can largely account for temperature compensation in wild-type plants and the temperaturespecific phenotypes of gi mutants.

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Section: Discussionsupporting

confidence: 81%

The Molecular Basis of Temperature Compensation in the Arabidopsis Circadian Clock

et al. 2006

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“…PER L1 ͞TIM protein-protein interactions are temperature-sensitive in a yeast assay (41), so perhaps the mps2 and mps5 transgenes produce defective PER-TIM dimerization (but see ref. 42). In addition, it may be more than coincidence that the frq 3 and frq 7 mutations in Neurospora crassa, which disrupt the temperature compensation of the circadian period, map to the immediate flanking regions of the fungal Thr-Gly͞Ser-Gly motif (43).…”

Section: Figmentioning

confidence: 99%

Molecular coevolution within a Drosophila clock gene

Peixoto

Hennessy

Townson

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

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The period (per) gene in Drosophila melanogaster provides an integral component of biological rhythmicity and encodes a protein that includes a repetitive threonineglycine (Thr-Gly) tract. Similar repeats are found in the frq and wc2 clock genes of Neurospora crassa and in the mammalian per homologues, but their circadian functions are unknown. In Drosophilids, the length of the Thr-Gly repeat varies widely between species, and sequence comparisons have suggested that the repeat length coevolves with the immediately f lanking amino acids. A functional test of the coevolution hypothesis was performed by generating several hybrid per transgenes between Drosophila pseudoobscura and D. melanogaster, whose repetitive regions differ in length by about 150 amino acids. The positions of the chimeric junctions were slightly altered in each transgene. Transformants carrying per constructs in which the repeat of one species was juxtaposed next to the f lanking region of the other were almost arrhythmic or showed a striking temperature sensitivity of the circadian period. In contrast, transgenes in which the repeat and f lanking regions were conspecific gave wild-type levels of circadian rescue. These results support the coevolutionary interpretation of the interspecific sequence changes in this region of the PER molecule and reveal a functional dimension to this process related to the clock's temperature compensation.

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“…This flexible-yetrobust characteristic is evolutionarily conserved in organisms ranging from photosynthetic bacteria to warm-blooded mammals (3,(10)(11)(12), and has interested researchers from a broad range of disciplines. However, despite many genetic and molecular studies (13)(14)(15)(16)(17)(18)(19)(20)(21)(22), the detailed biochemical mechanism underlying this characteristic remains poorly elucidated (3).…”

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confidence: 99%

CKIε/δ-dependent phosphorylation is a temperature-insensitive, period-determining process in the mammalian circadian clock

Isojima

Nakajima

Ukai

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

238

271

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T he circadian clock is a molecular mechanism underlying endogenous, self-sustained oscillations with a period of Ϸ24 h, manifested in diverse physiological and metabolic processes (1-3). The most striking feature of circadian clock is its flexible yet robust response to various environmental conditions. For example, circadian periodicity varies with light intensity (4-6) while remaining robust over a wide range of temperatures (''temperature compensation'') (1, 3, 7-9). This flexible-yetrobust characteristic is evolutionarily conserved in organisms ranging from photosynthetic bacteria to warm-blooded mammals (3, 10-12), and has interested researchers from a broad range of disciplines. However, despite many genetic and molecular studies (13-22), the detailed biochemical mechanism underlying this characteristic remains poorly elucidated (3).The simplest explanation for this flexible-yet-robust property is that the key period-determining reactions are insensitive to temperature but responsive to other environmental conditions. Indeed, Pittendrigh proposed the existence of a temperatureinsensitive component in the clock system in 1954 (7), and in 1968, he and his colleagues demonstrated that both the wave form and the period of circadian oscillations are invariant with temperature (23). However, the idea of a temperatureinsensitive biochemical reaction is counterintuitive, as elementary chemical processes are highly temperature-sensitive. One exception is the cyanobacterial clock, in which temperatureinsensitive enzymatic reactions are observed (24,25). However, the cyanobacterial clock is quite distinct from other clock systems, and this biochemical mechanism has not been demonstrated in other clocks.Recently, a chemical-biological approach was proposed to help elucidate the basic processes underlying circadian clocks (26), and high-throughput screening of a large chemical compound library was performed (27). In this report, to analyze systematically the fundamental processes involved in determining the period length of mammalian clocks, we tested 1,260 pharmacologically active compounds for their effect on period length in mouse and human clock cell lines, and found 10 compounds that most markedly lengthened the period of both clock cell lines affected both the central and peripheral circadian clocks. Most compounds inhibited CKI or CKI␦ activity, suggesting that CKI /␦-dependent phosphorylation is an important period-determining process in the mammalian circadian clock. Surprisingly, the degradation rate of endogenous PER2, which is regulated by CKI -dependent phosphorylation (28) and probably by CKI␦-dependent phosphorylation, was temperatureinsensitive in the living clock cells, and the temperatureinsensitivity was preserved even for the in vitro CKI /␦-dependent phosphorylation of a synthetic peptide derived from PER2. These results suggest that this period-determining process is flexible in response to chemical perturbation yet robust in the face of temperature perturbations. Based on these findings, we prop...

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The tim Mutant of the Drosophila Rhythm Gene timeless Manifests Allele-Specific Interactions with period Gene Mutants

Cited by 96 publications

References 30 publications

The Molecular Basis of Temperature Compensation in the Arabidopsis Circadian Clock

The Molecular Basis of Temperature Compensation in the Arabidopsis Circadian Clock

Molecular coevolution within a Drosophila clock gene

CKIε/δ-dependent phosphorylation is a temperature-insensitive, period-determining process in the mammalian circadian clock

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