Evidence map›Paper›PMID 29028801›Full record

ArticlePLoS genetics2017

dOCRL maintains immune cell quiescence by regulating endosomal traffic.

Steven J Del Signore, Sarah A Biber, Katherine S Lehmann, Stephanie R Heimler, Benjamin H Rosenfeld, Tania L Eskin, Sean T Sweeney, Avital A Rodal

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Modelling Lowe syndrome and Dent-2 disease using zebrafish.Frontiers in cell and developmental biology · 2025
    Review
  5. Article
  6. TheeLife · 2022
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. PTEN reduces endosomal PtdIns(4,5)PThe Journal of cell biology · 2019
    Article
  13. IPIP27 Coordinates PtdIns(4,5)PCurrent biology : CB · 2019
    Article
  14. 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

8 authors at 2 institutions in 2 countries.

Steven J Del SignoreRosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, Massachusetts, United States of America.
Sarah A BiberRosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, Massachusetts, United States of America.
Katherine S LehmannRosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, Massachusetts, United States of America.
Stephanie R HeimlerRosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, Massachusetts, United States of America.
Benjamin H RosenfeldRosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, Massachusetts, United States of America.
Tania L EskinRosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, Massachusetts, United States of America.
Sean T SweeneyDepartment of Biology, University of York, York, United Kingdom.ORCID http://orcid.org/0000-0003-2673-9578
Avital A RodalRosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, Massachusetts, United States of America.ORCID http://orcid.org/0000-0002-2051-8304
Brandeis University · USUniversity of York · GB

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Quantitative Neuroscience: Tools for Bridging Levels of AnalysisT32NS007292 · NINDS · BRANDEIS UNIVERSITY · PI GINA G TURRIGIANO · 1986 to 2026
$12.7M
DROSOPHILA GENOMICS RESOURCE CENTERP40OD010949 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Andrew Zelhof · 2012 to 2026
$9.4M
Medical Research Council MR/M013596/1NIH HHS P40 OD010949NIH HHS P40 OD018537NINDS NIH HHS T32 NS007292
6 · The paper itself

Abstract

Lowe Syndrome is a developmental disorder characterized by eye, kidney, and neurological pathologies, and is caused by mutations in the phosphatidylinositol-5-phosphatase OCRL. OCRL plays diverse roles in endocytic and endolysosomal trafficking, cytokinesis, and ciliogenesis, but it is unclear which of these cellular functions underlie specific patient symptoms. Here, we show that mutation of Drosophila OCRL causes cell-autonomous activation of hemocytes, which are macrophage-like cells of the innate immune system. Among many cell biological defects that we identified in docrl mutant hemocytes, we pinpointed the cause of innate immune cell activation to reduced Rab11-dependent recycling traffic and concomitantly increased Rab7-dependent late endosome traffic. Loss of docrl amplifies multiple immune-relevant signals, including Toll, Jun kinase, and STAT, and leads to Rab11-sensitive mis-sorting and excessive secretion of the Toll ligand Spåtzle. Thus, docrl regulation of endosomal traffic maintains hemocytes in a poised, but quiescent state, suggesting mechanisms by which endosomal misregulation of signaling may contribute to symptoms of Lowe syndrome.

Indexed as

AnimalsCytokinesisDrosophilaEndosomesHemocytesHumansImmunity, InnateMutationOculocerebrorenal SyndromePhosphoric Monoester HydrolasesProtein BindingOCRL protein, humanPhosphoric Monoester Hydrolases

Identifiers

PMID29028801
PMCPMC5656325
OpenAlexW2762441433

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.