Evidence map›Paper›PMID 31587092›Full record

ArticleCellular and molecular life sciences : CMLS2020

ESCRT-III-associated proteins and spastin inhibit protrudin-dependent polarised membrane traffic.

James W Connell, Rachel J Allison, Catherine E Rodger, Guy Pearson, Eliska Zlamalova, Evan Reid

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. IST1 regulates select recycling pathways.Traffic (Copenhagen, Denmark) · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. The Role of Spastin in Axon Biology.Frontiers in cell and developmental biology · 2022
    Review
  14. Article
  15. Review
  16. Review
  17. Final Exon Frameshift BiallelicBrain sciences · 2021
    Article
  18. Review
  19. Article
  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

6 authors at 1 institution in 1 country.

James W ConnellDepartment of Medical Genetics and Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK.
Rachel J AllisonDepartment of Medical Genetics and Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK.
Catherine E RodgerDepartment of Medical Genetics and Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK.
Guy PearsonDepartment of Medical Genetics and Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK.
Eliska ZlamalovaDepartment of Medical Genetics and Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK.
Evan ReidDepartment of Medical Genetics and Cambridge Institute for Medical Research, The Keith Peters Building, Cambridge Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK. ealr4@cam.ac.uk.ORCID http://orcid.org/0000-0003-1623-7304
University of Cambridge · GB

Funding

Medical Research Council MR/K50127X/1Medical Research Council MR/M00046X/1Medical Research Council MR/R026440/1Wellcome TrustWellcome Trust 082381Wellcome Trust 093026Wellcome Trust 100140
6 · The paper itself

Abstract

Mutations in the gene encoding the microtubule severing ATPase spastin are the most frequent cause of hereditary spastic paraplegia, a genetic condition characterised by length-dependent axonal degeneration. Here, we show that HeLa cells lacking spastin and embryonic fibroblasts from a spastin knock-in mouse model become highly polarised and develop cellular protrusions. In HeLa cells, this phenotype was rescued by wild-type spastin, but not by forms unable to sever microtubules or interact with endosomal ESCRT-III proteins. Cells lacking the spastin-interacting ESCRT-III-associated proteins IST1 or CHMP1B also developed protrusions. The protrusion phenotype required protrudin, a RAB-interacting protein that interacts with spastin and localises to ER-endosome contact sites, where it promotes KIF5-dependent endosomal motility to protrusions. Consistent with this, the protrusion phenotype in cells lacking spastin also required KIF5. Lack or mutation of spastin resulted in functional consequences for receptor traffic of a pathway implicated in HSP, as Bone Morphogenetic Protein receptor distribution became polarised. Our results, therefore, identify a novel role for ESCRT-III proteins and spastin in regulating polarised membrane traffic.

Indexed as

AnimalsBone Morphogenetic Protein ReceptorsCell MembraneCell PolarityCells, CulturedCell Surface ExtensionsEndosomal Sorting Complexes Required for TransportFibroblastsGene Knock-In TechniquesHeLa CellsHumansKinesinsMiceProtein TransportSpastic Paraplegia, HereditarySpastinBone Morphogenetic Protein ReceptorsEndosomal Sorting Complexes Required for TransportKIF5A protein, humanKinesinsSpastinSPAST protein, humanSpast protein, mouseVesicular Transport ProteinsZFYVE27 protein, humanAAA ATPaseAxonopathyBone morphogenetic protein signallingMicrotubule modificationProtrusion formation

Identifiers

PMID31587092
PMCPMC7320071
OpenAlexW2978328443

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.