Evidence map›Paper›PMID 27248654›Full record

ArticleOpen biology2016

ESCRT-II controls retinal axon growth by regulating DCC receptor levels and local protein synthesis.

Filip A Konopacki, Hovy Ho-Wai Wong, Asha Dwivedy, Anaïs Bellon, Michael D Blower, Christine E Holt

Open access · goldAbstract read
In one paragraph

Article in Open biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  5. The Role of Dynamic miRISC During Neuronal Development.Frontiers in molecular biosciences · 2020
    Review
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  7. Article
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  11. Article
  12. Review
  13. The RNA-binding complex ESCRT-II inThe Journal of biological chemistry · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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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.

Filip A KonopackiDepartment of Physiology Development Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3DY, UK.
Hovy Ho-Wai WongDepartment of Physiology Development Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3DY, UK.ORCID http://orcid.org/0000-0003-3317-478X
Asha DwivedyDepartment of Physiology Development Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3DY, UK.
Anaïs BellonDepartment of Physiology Development Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3DY, UK.
Michael D BlowerDepartment of Molecular Biology, Harvard Medical School, Simches Research Center, Boston, MA 02114, USA.
Christine E HoltDepartment of Physiology Development Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3DY, UK ceh33@cam.ac.uk.ORCID http://orcid.org/0000-0003-2829-121X
University of Cambridge · GBHarvard University · US

Funding

European Research Council 322817Wellcome TrustWellcome Trust 085314
6 · The paper itself

Abstract

Endocytosis and local protein synthesis (LPS) act coordinately to mediate the chemotropic responses of axons, but the link between these two processes is poorly understood. The endosomal sorting complex required for transport (ESCRT) is a key regulator of cargo sorting in the endocytic pathway, and here we have investigated the role of ESCRT-II, a critical ESCRT component, in Xenopus retinal ganglion cell (RGC) axons. We show that ESCRT-II is present in RGC axonal growth cones (GCs) where it co-localizes with endocytic vesicle GTPases and, unexpectedly, with the Netrin-1 receptor, deleted in colorectal cancer (DCC). ESCRT-II knockdown (KD) decreases endocytosis and, strikingly, reduces DCC in GCs and leads to axon growth and guidance defects. ESCRT-II-depleted axons fail to turn in response to a Netrin-1 gradient in vitro and many axons fail to exit the eye in vivo These defects, similar to Netrin-1/DCC loss-of-function phenotypes, can be rescued in whole (in vitro) or in part (in vivo) by expressing DCC. In addition, ESCRT-II KD impairs LPS in GCs and live imaging reveals that ESCRT-II transports mRNAs in axons. Collectively, our results show that the ESCRT-II-mediated endocytic pathway regulates both DCC and LPS in the axonal compartment and suggest that ESCRT-II aids gradient sensing in GCs by coupling endocytosis to LPS.

Indexed as

Protein BiosynthesisAnimalsAxonsDCC ReceptorEndocytosisEndosomal Sorting Complexes Required for TransportEndosomesGene Knockdown TechniquesGrowth ConesNerve Growth FactorsNetrin-1PhenotypeReceptors, Cell SurfaceRetinaRetinal Ganglion CellsRNA, MessengerDCC protein, XenopusDCC ReceptorEndosomal Sorting Complexes Required for TransportNerve Growth FactorsNetrin-1Receptors, Cell SurfaceRNA, MessengerTumor Suppressor ProteinsXenopus Proteinsaxon guidanceDCCendocytosisESCRTNetrin-1protein synthesis

Identifiers

PMID27248654
PMCPMC4852451
OpenAlexW2341733057

What OpenQuestion holds

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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.