Evidence map›Paper›PMID 21059886›Full record

ArticleGenetics2011

Central regulation of locomotor behavior of Drosophila melanogaster depends on a CASK isoform containing CaMK-like and L27 domains.

Justin B Slawson, Elena A Kuklin, Aki Ejima, Konark Mukherjee, Lilly Ostrovsky, Leslie C Griffith

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. CASK hypomorph mice display cone photoreceptor dysfunction.bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Review
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  15. Review
  16. Article
  17. Neural functions of long noncoding RNAs in Drosophila.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2015
    Review
  18. Article
  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 2 institutions in 2 countries.

Justin B SlawsonDepartment of Biology, Volen Center for Complex Systems and National Center for Behavioral Genomics, Brandeis University, Waltham, Massachusetts 02454-9110, USA.
Elena A Kuklin
Aki Ejima
Konark Mukherjee
Lilly Ostrovsky
Leslie C Griffith
Brandeis University · USKyoto University · JP

Funding

NEUROCHEMISTRY AND GENETICS OF DROSOPHILA CAM KINASE IIR01GM054408 · NIGMS · BRANDEIS UNIVERSITY · PI GRIFFITH, LESLIE C · 1996 to 2014
$5.0M
The Behavioral Role and Synpatic Localization of dCASK in Drosophila melanogasterF31NS064679 · NINDS · BRANDEIS UNIVERSITY · PI SLAWSON, JUSTIN · 2009 to 2011
$58k
NIGMS NIH HHS R01 GM054408NIGMS NIH HHS R01GM54408NINDS NIH HHS F31 NS064679NINDS NIH HHS F31 NS064679-01A1
6 · The paper itself

Abstract

Genetic causes for disturbances of locomotor behavior can be due to muscle, peripheral neuron, or central nervous system pathologies. The Drosophila melanogaster homolog of human CASK (also known as caki or camguk) is a molecular scaffold that has been postulated to have roles in both locomotion and plasticity. These conclusions are based on studies using overlapping deficiencies that largely eliminate the entire CASK locus, but contain additional chromosomal aberrations as well. More importantly, analysis of the sequenced Drosophila genome suggests the existence of multiple protein variants from the CASK locus, further complicating the interpretation of experiments using deficiency strains. In this study, we generated small deletions within the CASK gene that eliminate gene products containing the CaMK-like and L27 domains (CASK-β), but do not affect transcripts encoding the smaller forms (CASK-α), which are structurally homologous to vertebrate MPP1. These mutants have normal olfactory habituation, but exhibit a striking array of locomotor problems that includes both initiation and motor maintenance defects. Previous studies had suggested that presynaptic release defects at the neuromuscular junction in the multigene deficiency strain were the likely basis of its locomotor phenotype. The locomotor phenotype of the CASK-β mutant, however, cannot be rescued by expression of a CASK-β transgene in motor neurons. Expression in a subset of central neurons that does not include the ellipsoid body, a well-known pre-motor neuropil, provides complete rescue. Full-length CASK-β, while widely expressed in the nervous system, appears to have a unique role within central circuits that control motor output.

Indexed as

Motor ActivityAnimalsBrainChromosome MappingCircadian RhythmCourtshipDrosophila melanogasterFemaleGene Expression Regulation, EnzymologicGenetic LociGuanylate KinasesHabituation, PsychophysiologicIsoenzymesMaleMutagenesisPheromonesCASK kinasesGuanylate KinasesIsoenzymesPheromonesProtein KinasesRNA, Messenger

Identifiers

PMID21059886
PMCPMC3018317
OpenAlexW2096754870

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.