ArticleJournal of cell science2022
The retromer complex regulates C. elegans development and mammalian ciliogenesis.
Article in Journal of cell science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- A Quarter Century of EHD Protein Research: From Endosomal Recycling to Ciliopathies.Traffic (Copenhagen, Denmark) · 2026Review
- Article
- Membrane stability under heat stress: molecular signaling, lipid remodeling, and defense mechanisms in plants.Plant cell reports · 2026Review
- A commercially available DJ-1 antibody does not detectmicroPublication biology · 2026Article
- Mutant mice with rod-specific VPS35 deletion exhibit retinal α-synuclein pathology-associated degeneration.Nature communications · 2024Article
- Emerging insights into CP110 removal during early steps of ciliogenesis.Journal of cell science · 2024Review
- Article
- EHD1 promotes CP110 ubiquitination by centriolar satellite delivery of HERC2 to the mother centriole.EMBO reports · 2023Article
- Canonical and Non-Canonical Roles of SNX1 and SNX2 in Endosomal Membrane Dynamics.Contact (Thousand Oaks (Ventura County, Calif.))Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The mammalian retromer consists of subunits VPS26 (either VPS26A or VPS26B), VPS29 and VPS35, and a loosely associated sorting nexin (SNX) heterodimer or a variety of other SNX proteins. Despite involvement in yeast and mammalian cell trafficking, the role of retromer in development is poorly understood, and its impact on primary ciliogenesis remains unknown. Using CRISPR/Cas9 editing, we demonstrate that vps-26-knockout worms have reduced brood sizes, impaired vulval development and decreased body length, all of which have been linked to ciliogenesis defects. Although preliminary studies did not identify worm ciliary defects, and impaired development limited additional ciliogenesis studies, we turned to mammalian cells to investigate the role of retromer in ciliogenesis. VPS35 localized to the primary cilium of mammalian cells, and depletion of VPS26, VPS35, VPS29, SNX1, SNX2, SNX5 or SNX27 led to decreased ciliogenesis. Retromer also coimmunoprecipitated with the centriolar protein, CP110 (also known as CCP110), and was required for its removal from the mother centriole. Herein, we characterize new roles for retromer in C. elegans development and in the regulation of ciliogenesis in mammalian cells, suggesting a novel role for retromer in CP110 removal from the mother centriole.
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Registered trials
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 Socratic graph.