ArticleThe Journal of cell biology2025
A collagen IV fluorophore knock-in toolkit reveals trimer diversity in C. elegans basement membranes.
Article in The Journal of cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Zebrafish knock-in lines enabling live visualization of extracellular matrix dynamics during development and regeneration.Development (Cambridge, England) · 2026Article
- WormTagDB: a systematic survey of endogenously tagged proteins in Caenorhabditis elegans and roadmap toward the tagged proteome.G3 (Bethesda, Md.) · 2026Article
- Specialized high-capacity mitochondria fuel cell invasion.Current biology : CB · 2026Article
- WormTagDB: A Systematic Survey of Endogenously Tagged Proteins inbioRxiv : the preprint server for biology · 2025Article
- Live visualization of extracellular matrix dynamics during development and regeneration in zebrafish.bioRxiv : the preprint server for biology · 2025Article
- A switch in collagen expression regulates cessation of distal tip cell migration inbioRxiv : the preprint server for biology · 2025Article
- The life cycle of type IV collagen.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The type IV collagen triple helix, composed of three ⍺-chains, is a core basement membrane (BM) component that assembles into a network within BMs. Endogenous tagging of all ⍺-chains with genetically encoded fluorophores has remained elusive, limiting our understanding of this crucial BM component. Through genome editing, we show that the C termini of the C. elegans type IV collagen ⍺-chains EMB-9 and LET-2 can be fused to a variety of fluorophores to create a strain toolkit with wild-type health. Using quantitative imaging, our results suggest a preference for LET-2-LET-2-EMB-9 trimer construction, but also tissue-specific flexibility in trimers assembled driven by differences in ⍺-chain expression levels. By tagging emb-9 and let-2 mutants that model human Gould syndrome, a complex multitissue disorder, we further discover defects in extracellular accumulation and turnover that might help explain disease pathology. Together, our findings identify a permissive tagging site in C. elegans that will allow diverse studies on type IV collagen regulation and function in animals.
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