ArticlePLoS genetics2013
Clathrin and AP2 are required for phagocytic receptor-mediated apoptotic cell clearance in Caenorhabditis elegans.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Ubiquitination of LMP-1 by UFD-2 regulates apoptotic cell clearance.Cell death and differentiation · 2026Article
- Unlocking the black box: multimodal imaging and quantitative analysis of plant vesicular trafficking.Advanced biotechnology · 2026Review
- AP2: an indispensable host factor in virus infection.Journal of virology · 2026Review
- CED-6/GULP and components of the clathrin-mediated endocytosis machinery act redundantly to correctly display CED-1 on the cell membrane in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2024Article
- Intestinal cell diversity and treatment responses in a parasitic nematode at single cell resolution.BMC genomics · 2024Article
- VAMP5 promotes Fcγ receptor-mediated phagocytosis and regulates phagosome maturation in macrophages.Molecular biology of the cell · 2024Article
- Transcriptomics reveal a unique phago-mixotrophic response to low nutrient concentrations in the prasinophyteISME communications · 2024Article
- The recurrent pathogenic Pro890Leu substitution in CLTC causes a generalized defect in synaptic transmission inFrontiers in molecular neuroscience · 2023Article
- Review
- Article
- The Ubiquitin-Proteasome System in Apoptosis and Apoptotic Cell Clearance.Frontiers in cell and developmental biology · 2022Review
- Response of G protein-coupled receptor CED-1 in germline to polystyrene nanoparticles inNanoscale advances · 2021Article
- SUMO modification in apoptosis.Journal of molecular histology · 2021Review
- Degron-tagged reporters probe membrane topology and enable the specific labelling of membrane-wrapped structures.Nature communications · 2019Article
- Dynein links engulfment and execution of apoptosis via CED-4/Apaf1 in C. elegans.Cell death & disease · 2018Article
- WDR91 is a Rab7 effector required for neuronal development.The Journal of cell biology · 2017Article
- Developmentally programmed germ cell remodelling by endodermal cell cannibalism.Nature cell biology · 2016Article
- Article
- How antibodies alter the cell entry pathway of dengue virus particles in macrophages.Scientific reports · 2016Article
- Programmed cell death and clearance of cell corpses in Caenorhabditis elegans.Cellular and molecular life sciences : CMLS · 2016Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clathrin and the multi-subunit adaptor protein complex AP2 are central players in clathrin-mediated endocytosis by which the cell selectively internalizes surface materials. Here, we report the essential role of clathrin and AP2 in phagocytosis of apoptotic cells. In Caenorhabditis elegans, depletion of the clathrin heavy chain CHC-1 and individual components of AP2 led to a significant accumulation of germ cell corpses, which resulted from defects in both cell corpse engulfment and phagosome maturation required for corpse removal. CHC-1 and AP2 components associate with phagosomes in an inter-dependent manner. Importantly, we found that the phagocytic receptor CED-1 interacts with the α subunit of AP2, while the CED-6/Gulp adaptor forms a complex with both CHC-1 and the AP2 complex, which likely mediates the rearrangement of the actin cytoskeleton required for cell corpse engulfment triggered by the CED-1 signaling pathway. In addition, CHC-1 and AP2 promote the phagosomal association of LST-4/Snx9/18/33 and DYN-1/dynamin by forming a complex with them, thereby facilitating the maturation of phagosomes necessary for corpse degradation. These findings reveal a non-classical role of clathrin and AP2 and establish them as indispensable regulators in phagocytic receptor-mediated apoptotic cell clearance.
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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.