Evidence map›Paper›PMID 17369364›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Impaired clock output by altered connectivity in the circadian network.

María de la Paz Fernández, Jessie Chu, Adriana Villella, Nigel Atkinson, Steve A Kay, María Fernanda Ceriani

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

36 citing papers in PubMed, 58 citations in OpenAlex.

  1. Journal of biological rhythms · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Intermediate conductance CaFrontiers in insect science · 2022
    Article
  6. Review
  7. The E3 ubiquitin ligase adaptorProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  8. Impaired Pre-Motor Circuit Activity and Movement in a Drosophila Model of KCNMA1-Linked Dyskinesia.Movement disorders : official journal of the Movement Disorder Society · 2021
    Article
  9. High-Frequency Neuronal Bursting is Essential for Circadian and Sleep Behaviors inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. BKCells · 2019
    Article
  15. Article
  16. Article
  17. Article
  18. BK Channels in the Central Nervous System.International review of neurobiology · 2016
    Review
  19. Article
  20. 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

6 authors at 4 institutions in 2 countries.

María de la Paz FernándezLaboratorio de Genética del Comportamiento, Fundación Instituto Leloir, Av. Patricias Argentinas 435, 1405 Buenos Aires, Argentina.
Jessie Chu
Adriana Villella
Nigel Atkinson
Steve A Kay
María Fernanda Ceriani
Fundación Instituto Leloir · ARScripps Research Institute · USBrandeis University · USThe University of Texas at Austin · US

Funding

Circadian control of behavior in DrosophilaR03TW005998 · FIC · SCRIPPS RESEARCH INSTITUTE · PI KAY, STEVE A · 2002 to 2004
$166k
FIC NIH HHS R03 TW005998FIC NIH HHS R03TW005998-01
6 · The paper itself

Abstract

Substantial progress has been made in elucidating the molecular processes that impart a temporal control to physiology and behavior in most eukaryotes. In Drosophila, dorsal and ventral neuronal networks act in concert to convey rhythmicity. Recently, the hierarchical organization among the different circadian clusters has been addressed, but how molecular oscillations translate into rhythmic behavior remains unclear. The small ventral lateral neurons can synchronize certain dorsal oscillators likely through the release of pigment dispersing factor (PDF), a neuropeptide central to the control of rhythmic rest-activity cycles. In the present study, we have taken advantage of flies exhibiting a distinctive arrhythmic phenotype due to mutation of the potassium channel slowpoke (slo) to examine the relevance of specific neuronal populations involved in the circadian control of behavior. We show that altered neuronal function associated with the null mutation specifically impaired PDF accumulation in the dorsal protocerebrum and, in turn, desynchronized molecular oscillations in the dorsal clusters. However, molecular oscillations in the small ventral lateral neurons are properly running in the null mutant, indicating that slo is acting downstream of these core pacemaker cells, most likely in the output pathway. Surprisingly, disrupted PDF signaling by slo dysfunction directly affects the structure of the underlying circuit. Our observations demonstrate that subtle structural changes within the circadian network are responsible for behavioral arrhythmicity.

Indexed as

Circadian RhythmAnimalsBehavior, AnimalBiological ClocksDrosophila melanogasterDrosophila ProteinsFemaleMaleMutationNeuronsNeuropeptidesOscillometryPhenotypeSignal TransductionTransgenesDrosophila ProteinsNeuropeptides

Identifiers

PMID17369364
PMCPMC1838506
OpenAlexW1966657605

What OpenQuestion holds

Textmetadata
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.