ArticleGenetics2005
The novel Drosophila tim(blind) mutation affects behavioral rhythms but not periodic eclosion.
Article in Genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Coevolution ofiScience · 2025Article
- A Compensated Clock: Temperature and Nutritional Compensation Mechanisms Across Circadian Systems.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Evolution of casein kinase 1 and functional analysis of newFrontiers in physiology · 2022Article
- NewFrontiers in physiology · 2019Article
- Identification of Light-Sensitive Phosphorylation Sites on PERIOD That Regulate the Pace of Circadian Rhythms in Drosophila.Molecular and cellular biology · 2015Article
- Role for circadian clock genes in seasonal timing: testing the Bünning hypothesis.PLoS genetics · 2014Article
- A role for the PERIOD:PERIOD homodimer in the Drosophila circadian clock.PLoS biology · 2009Article
- Article
- Moonlight shifts the endogenous clock of Drosophila melanogaster.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Veela defines a molecular link between Cryptochrome and Timeless in the light-input pathway to Drosophila's circadian clock.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Disruption of Cryptochrome partially restores circadian rhythmicity to the arrhythmic period mutant of Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Circadian clock function depends on the tightly regulated exclusion or presence of clock proteins within the nucleus. A newly induced long-period timeless mutant, tim(blind), encodes a constitutively hypophosphorylated TIM protein. The mutant protein is not properly degraded by light, and tim(blind) flies show abnormal behavioral responses to light pulses. This is probably caused by impaired nuclear accumulation of TIM(BLIND) protein, which we observed in brain pacemaker neurons and photoreceptor cells of the compound eye. tim(blind) encodes two closely spaced amino acid changes compared to the wild-type TIM protein; one of them is within a putative nuclear export signal of TIM. Under constant conditions, tim(blind) flies exhibit 26-hr free-running locomotor rhythms, which are not correlated with a period lengthening of eclosion rhythms and period-luciferase reporter-gene oscillations. Therefore it seems possible that TIM--in addition to its well-established role as core clock factor--functions as a clock output factor, involved in determining the period length of adult locomotor rhythms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.