Evidence map›Paper›PMID 30220571›Full record

ArticleDevelopmental cell2018

RAB-35 and ARF-6 GTPases Mediate Engulfment and Clearance Following Linker Cell-Type Death.

Lena M Kutscher, Wolfgang Keil, Shai Shaham

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 33% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. bioRxiv : the preprint server for biology · 2026
    Article
  3. Non-apoptotic death of thebioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Cell death in animal development.Development (Cambridge, England) · 2020
    Review
  12. Article
  13. Article
  14. After-Death Functions of Cell Death.The Yale journal of biology and medicine · 2019
    Review
  15. 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

3 authors at 1 institution in 1 country.

Lena M KutscherLaboratory of Developmental Genetics, The Rockefeller University, New York, NY 10065, USA.
Wolfgang KeilLaboratory of Developmental Genetics, The Rockefeller University, New York, NY 10065, USA; Center for Studies in Physics and Biology, The Rockefeller University, New York, NY 10065, USA.
Shai ShahamLaboratory of Developmental Genetics, The Rockefeller University, New York, NY 10065, USA. Electronic address: shaham@rockefeller.edu.
Rockefeller University · US

Funding

Glial Control of Neuron Development and Function - Administrative SupplementR35NS105094 · NINDS · ROCKEFELLER UNIVERSITY · PI SHAHAM, SHAI · 2018 to 2025
$8.9M
Genetics and Cell BiologyT32GM066699 · NIGMS · ROCKEFELLER UNIVERSITY · PI STRICKLAND, SIDNEY · 2004 to 2021
$7.6M
Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Control of nonapoptotic C. elegans cell death similar to neurodegenerationR01NS081490 · NINDS · ROCKEFELLER UNIVERSITY · PI SHAHAM, SHAI · 2012 to 2017
$2.2M
Control of Linker Cell Death in C. elegansR01HD078703 · NICHD · ROCKEFELLER UNIVERSITY · PI SHAHAM, SHAI · 2014 to 2018
$1.7M
NICHD NIH HHS R01 HD078703NIGMS NIH HHS T32 GM066699NIH HHS P40 OD010440NINDS NIH HHS R01 NS081490NINDS NIH HHS R35 NS105094
6 · The paper itself

Abstract

Clearance of dying cells is essential for development and homeostasis. Conserved genes mediate apoptotic cell removal, but whether these genes control non-apoptotic cell removal is a major open question. Linker cell-type death (LCD) is a prevalent non-apoptotic developmental cell death process with features conserved from C. elegans to vertebrates. Using microfluidics-based long-term in vivo imaging, we show that unlike apoptotic cells, the C. elegans linker cell, which dies by LCD, is competitively phagocytosed by two neighboring cells, resulting in cell splitting. Subsequent cell elimination does not require apoptotic engulfment genes. Rather, we find that RAB-35 GTPase is a key coordinator of competitive phagocytosis onset and cell degradation. RAB-35 binds CNT-1, an ARF-6 GTPase activating protein, and removes ARF-6, a degradation inhibitor, from phagosome membranes. This facilitates phosphatidylinositol-4,5-bisphosphate removal from phagosome membranes, promoting phagolysosome maturation. Our studies suggest that RAB-35 and ARF-6 drive a conserved program eliminating cells dying by LCD.

Indexed as

AnimalsApoptosisCaenorhabditis elegansCaenorhabditis elegans ProteinsCell DeathGTPase-Activating ProteinsHomeostasisIntracellular MembranesPhagocytosisPhagosomesPhosphatidylinositol 4,5-DiphosphatePhosphatidylinositolsrab GTP-Binding ProteinsCaenorhabditis elegans ProteinsCNT-1 protein, C elegansGTPase-Activating ProteinsPhosphatidylinositol 4,5-DiphosphatePhosphatidylinositolsRab-35 protein, C elegansrab GTP-Binding ProteinsARF-6C. eleganscompetitive phagocytosisLCDlinker celllinker cell-type deathnon-apoptoticphagocytosisphagosome maturationRAB-35

Identifiers

PMID30220571
PMCPMC6200590
OpenAlexW2784683067

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.