Evidence map›Paper›PMID 28158614›Full record

ArticleHuman molecular genetics2017

LRRK2(I2020T) functional genetic interactors that modify eye degeneration and dopaminergic cell loss in Drosophila.

Paul C Marcogliese, Sameera Abuaish, Ghassan Kabbach, Elizabeth Abdel-Messih, Sarah Seang, Gang Li, Ruth S Slack, M Emdadul Haque, Katerina Venderova, David S Park

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Parkinson's Disease: Exploring Different Animal Model Systems.International journal of molecular sciences · 2023
    Review
  3. G3 (Bethesda, Md.) · 2020
    Article
  4. Review
  5. IRF2BPL Is Associated with Neurological Phenotypes.American journal of human genetics · 2018
    Article
  6. Article
  7. Regulation of myeloid cell phagocytosis by LRRK2 via WAVE2 complex stabilization is altered in Parkinson's disease.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  8. Review
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

10 authors at 3 institutions in 3 countries.

Paul C MarcoglieseDepartment of Cellular and Molecular Medicine.
Sameera AbuaishDepartment of Cellular and Molecular Medicine.
Ghassan KabbachDepartment of Cellular and Molecular Medicine.
Elizabeth Abdel-MessihDepartment of Cellular and Molecular Medicine.
Sarah SeangDepartment of Cellular and Molecular Medicine.
Gang LiDepartment of Cellular and Molecular Medicine.
Ruth S SlackDepartment of Cellular and Molecular Medicine.
M Emdadul HaqueDepartment of Biochemistry, College of Medicine and Health Science, United Arab Emirates University, Al Ain, UAE.
Katerina VenderovaDepartment of Biopharmaceutical Sciences, Keck Graduate Institute, Claremont, CA, USA.
David S ParkDepartment of Cellular and Molecular Medicine.
University of Ottawa · CAKeck Graduate Institute · USUnited Arab Emirates University · AE

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
NIH HHS P40 OD018537
6 · The paper itself

Abstract

Progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta is the primary cause for motor symptoms observed in Parkinson's disease (PD). Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most commonly linked contributor to familial PD. LRRK2 is suggested to be involved in a wide variety of cellular processes, but deciphering its role in the pathogenesis of PD has been difficult. Modelling PD in rodents has been a persistent challenge for the field. However, the fruit fly has been exploited to recapitulate PD gene related dopaminergic cell loss. Using the GAL4-UAS system and established models of hLRRK2 induced eye degeneration in Drosophila, we conducted an unbiased suppressor/enhancer screen to uncover genetic modifiers of LRRK2. We have identified 36 candidate interactors that modify LRRK2 induced toxicity in the Drosophila eye. Importantly, we determined that a subset of these interactors also modified hLRRK2(I2020T) induced dopaminergic neuronal loss in the fly brain and uncovered 16 candidates that modify dopaminergic cell loss. Our results suggest LRRK2 may be involved in a wide variety of cellular processes and the results from this screen provide an important genetic resource for further evaluation of LRRK2 function.

Indexed as

AnimalsDisease Models, AnimalDopamineDopaminergic NeuronsDrosophila melanogasterDrosophila ProteinsEpistasis, GeneticEye DiseasesHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2MiceMice, TransgenicMutationParkinson DiseaseProtein Serine-Threonine KinasesSubstantia NigraDopamineDrosophila ProteinsLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK protein, DrosophilaProtein Serine-Threonine Kinases

Identifiers

PMID28158614
PMCPMC6075539
OpenAlexW2583450464

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.