Evidence map›Paper›PMID 19755582›Full record

ArticleJournal of biological rhythms2009

Genetic analysis of ectopic circadian clock induction in Drosophila.

Valerie L Kilman, Ravi Allada

Open access · greenAbstract read
In one paragraph

Article in Journal of biological rhythms, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 41% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. CLOCK stabilizes CYCLE to initiate clock function inProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  4. Article
  5. Article
  6. Circadian Activators Are Expressed Days before They Initiate Clock Function in Late Pacemaker Neurons from Drosophila.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  7. Article
  8. Article
  9. Article
  10. Surprising gene expression patterns within and between PDF-containing circadian neurons in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Valerie L KilmanDepartment of Neurobiology and Physiology, Center for Sleep and Circadian Biology, Northwestern University, Evanston, Illinois 60208, USA. v-kilman@northwestern.edu
Ravi Allada
Northwestern University · US

Funding

Intercellular Signaling in the Circadian ClockR01NS059042 · NINDS · NORTHWESTERN UNIVERSITY · PI ALLADA, RAVI · 2008 to 2012
$1.6M
Function of the Novel Ion Channel narrow abdomen in Daily RhythmsR01NS052903 · NINDS · NORTHWESTERN UNIVERSITY · PI ALLADA, RAVI · 2005 to 2008
$1.3M
Induction of the Molecular Circadian ClockK01MH070456 · NIMH · NORTHWESTERN UNIVERSITY · PI KILMAN, VALERIE L · 2005 to 2009
$745k
NIMH NIH HHS K01 MH070456NINDS NIH HHS NS059042NINDS NIH HHS R01 NS052903NINDS NIH HHS R01 NS059042
6 · The paper itself

Abstract

Cell-autonomous feedback loops underlie the molecular oscillations that define circadian clocks. In Drosophila the transcription factor Clk activates multiple clock components of feedback loops many of which feed back and regulate Clk expression or activity. Previously the authors evoked similar molecular oscillations in putatively naïve neurons in Drosophila by ectopic expression of a single gene, Clk, suggesting a master regulator function. Using molecular oscillations of the core clock component PERIOD (PER), the authors observed dramatic and widespread molecular oscillations throughout the brain in flies expressing ectopic Clk. Consistent with the master regulator hypothesis, they found that Clk is uniquely capable of inducing ectopic clocks as ectopic induction of other clock components fails to induce circadian rhythms. Clk also induces oscillations even when expression is adult restricted, suggesting that ectopic clocks can even be induced in differentiated cells. However, if transgene expression is discontinued, PER expression disappears, indicating that Clk must be continually active to sustain ectopic clock function. In some cases Clk-mediated PER induction was observed without apparent synchronous cycling, perhaps due to desynchronization of rhythms between clocks or truly cell autonomous arrhythmic PER expression, indicating that additional factors may be necessary for coherent rhythms in cells ectopically expressing Clk. To determine minimal requirements for circadian clock induction by Clk, the authors determined the genetic requirements of ectopic clocks. No ectopic clocks are induced in mutants of Clk's heterodimeric partner cyc. In addition, noncycling PER is observed when ectopic Clk is induced in a cryb mutant background. While other factors may contribute, these results indicate that persistent Clock induction is uniquely capable of broadly inducing ectopic rhythms even in adults, consistent with a special role at the top of a clock gene hierarchy.

Indexed as

Gene Expression RegulationAnimalsARNTL Transcription FactorsBiological ClocksCircadian RhythmCLOCK ProteinsCryptochromesDrosophila melanogasterDrosophila ProteinsEye ProteinsPeriod Circadian ProteinsARNTL Transcription FactorsClk protein, DrosophilaCLOCK Proteinscry protein, DrosophilaCryptochromescyc protein, DrosophilaDrosophila ProteinsEye ProteinsPeriod Circadian ProteinsPER protein, Drosophilatim protein, Drosophila

Identifiers

PMID19755582
PMCPMC3033121
OpenAlexW2072456131

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.