Evidence map›Paper›PMID 22934826›Full record

ArticleTraffic (Copenhagen, Denmark)2012

Drosophila mauve mutants reveal a role of LYST homologs late in the maturation of phagosomes and autophagosomes.

Mokhlasur Rahman, Adam Haberman, Charles Tracy, Sanchali Ray, Helmut Krämer

Open access · greenAbstract read
In one paragraph

Article in Traffic (Copenhagen, Denmark), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Spectrum ofJournal of medical genetics · 2024
    Review
  5. Review
  6. The lysosomal trafficking regulator is necessary for normal wound healing.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Lysosomal size matters.Traffic (Copenhagen, Denmark) · 2020
    Review
  11. Article
  12. Review
  13. LRBA in the endomembrane system.Colombia medica (Cali, Colombia) · 2018
    Review
  14. Isolation and Infection ofBio-protocol · 2017
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

5 authors at 3 institutions in 1 country.

Mokhlasur RahmanDepartment of Neuroscience, UT Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9111, USA.
Adam Haberman
Charles Tracy
Sanchali Ray
Helmut Krämer
The University of Texas Southwestern Medical Center · USOberlin College · USSouthwestern Medical Center · US

Funding

MOLECULAR ANALYSIS OF THE BOSS TRANSMEMBRANE LIGANDR01EY010199 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI Helmut J Kramer · 1994 to 2026
$9.7M
NEI NIH HHS EY10199NEI NIH HHS R01 EY010199
6 · The paper itself

Abstract

Chediak-Higashi syndrome (CHS) is a lethal disease caused by mutations that inactivate the lysosomal trafficking regulator protein (LYST). Patients suffer from diverse symptoms including oculocutaneous albinism, recurrent infections, neutropenia and progressive neurodegeneration. These defects have been traced back to over-sized lysosomes and lysosome-related organelles (LROs) in different cell types. Here, we explore mutants in the Drosophila mauve gene as a new model system for CHS. The mauve gene (CG42863) encodes a large BEACH domain protein of 3535 amino acids similar to LYST. This reflects a functional homology between these proteins as mauve mutants also display enlarged LROs, such as pigment granules. This Drosophila model also replicates the enhanced susceptibility to infections and we show a defect in the cellular immune response. Early stages of phagocytosis proceed normally in mauve mutant hemocytes but, unlike in wild type, late phagosomes fuse and generate large vacuoles containing many bacteria. Autophagy is similarly affected in mauve fat bodies as starvation-induced autophagosomes grow beyond their normal size. Together these data suggest a model in which Mauve functions to restrict homotypic fusion of different pre-lysosomal organelles and LROs.

Indexed as

AnimalsAutophagyCytoplasmic GranulesDrosophilaDrosophila ProteinsEscherichia coliHemocytesImmunity, InnateLysosomesMutationOrganelle SizePhagocytosisPhagosomesVesicular Transport ProteinsDrosophila Proteinsmv protein, DrosophilaVesicular Transport Proteins

Identifiers

PMID22934826
PMCPMC3528838
OpenAlexW1565084043

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.