Evidence map›Paper›PMID 22041890›Full record

ArticleCell research2011

SNX3 controls Wingless/Wnt secretion through regulating retromer-dependent recycling of Wntless.

Peng Zhang, Yihui Wu, Tatyana Y Belenkaya, Xinhua Lin

Open access · hybridAbstract read
In one paragraph

Article in Cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

76 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The role of Evi/Wntless in exporting Wnt proteins.Development (Cambridge, England) · 2023
    Review
  10. Protein sorting from endosomes to the TGN.Frontiers in cell and developmental biology · 2023
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. The Emerging Mechanisms of Wnt Secretion and Signaling in Development.Frontiers in cell and developmental biology · 2021
    Review
  20. Review

16 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 2 countries.

Peng ZhangState Key Laboratory of Biomembrane and Membrane Biotechnology, and Key Laboratory of Stem Cell and Developmental Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.
Yihui Wu
Tatyana Y Belenkaya
Xinhua Lin
Institute of Zoology · CNChinese Academy of Sciences · CNCincinnati Children's Hospital Medical Center · US

Funding

Regulation of Wingless (Wg) Signaling and Morphogen Gradient FormationR01GM063891 · NIGMS · CINCINNATI CHILDRENS HOSP MED CTR · PI LIN, XINHUA · 2002 to 2015
$3.6M
Roles of Retromer Complex in DevelopmentR01GM087517 · NIGMS · CINCINNATI CHILDRENS HOSP MED CTR · PI LIN, XINHUA · 2010 to 2013
$1.1M
NIGMS NIH HHS 1R01GM087517NIGMS NIH HHS 2R01 GM063891NIGMS NIH HHS R01 GM063891NIGMS NIH HHS R01 GM087517
6 · The paper itself

Abstract

Drosophila Wingless (Wg) acts as a morphogen during development. Wg secretion is controlled by a seven-pass transmembrane cargo Wntless (Wls). We have recently identified retromer as a key regulator involved in Wls trafficking. As sorting nexin (SNX) molecules are essential components of the retromer complex, we hypothesized that specific SNX(s) is required for retromer-mediated Wnt secretion. Here, we generated Drosophila mutants for all of the eight snx members, and identified Drosophila SNX3 (DSNX3) as an essential molecule required for Wg secretion. We show that Wg secretion and its signaling activity are defective in Dsnx3 mutant clones in wing discs. Wg levels in the culture medium of Dsnx3-depleted S2 cells are also markedly reduced. Importantly, Wls levels are strikingly reduced in Dsnx3 mutant cells, and overexpression of Wls can rescue the Wg secretion defect observed in Dsnx3 mutant cells. Moreover, DSNX3 can interact with the retromer component Vps35, and co-localize with Vps35 in early endosomes. These data indicate that DSNX3 regulates Wg secretion via retromer-dependent Wls recycling. In contrast, we found that Wg secretion is not defective in cells mutant for Drosophila snx1 and snx6, two components of the classical retromer complex. Ectopic expression of DSNX1 or DSNX6 fails to rescue the Wg secretion defect in Dsnx3 mutant wing discs and in Dsnx3 dsRNA-treated S2 cells. These data demonstrate the specificity of the DSNX3-retromer complex in Wls recycling. Together, our findings suggest that DSNX3 acts as a cargo-specific component of retromer, which is required for endocytic recycling of Wls and Wg/Wnt secretion.

Indexed as

AnimalsCell LineDrosophilaDrosophila ProteinsEndosomesIntracellular Signaling Peptides and ProteinsMutationSignal TransductionSorting NexinsVesicular Transport ProteinsWnt1 ProteinWnt ProteinsDrosophila ProteinsIntracellular Signaling Peptides and ProteinsSorting NexinsVesicular Transport ProteinsVps35 protein, Drosophilawg protein, DrosophilaWls protein, DrosophilaWnt1 ProteinWnt Proteins

Identifiers

PMID22041890
PMCPMC3357989
OpenAlexW2049033721

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.