ArticlePLoS genetics2025
A defining member of the new cysteine-cradle family is an aECM protein signalling skin damage in C. elegans.
Article in PLoS genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Pathogen subversion of neuro-epidermal signaling impairs lysosomal function to disrupt collagen homeostasis in Caenorhabditis elegans.PLoS biology · 2026Article
- A Lipocalin and a Hedgehog-related protein are partners in thebioRxiv : the preprint server for biology · 2026Article
- Worming out defence strategies: mechanisms of immunity through the lens of genetic screens in C. elegans.Heredity · 2026Review
- Pre-cuticle DPY-6 acts as a blueprint for aECM periodic organization inbioRxiv : the preprint server for biology · 2026Article
- Pre-cuticle DPY-6 acts as a blueprint for aECM periodic organization in C. elegans.PLoS genetics · 2026Article
- Multiscale patterning of a model apical extracellular matrix revealed by systematic endogenous protein tagging.bioRxiv : the preprint server for biology · 2025Article
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Abstract
Apical extracellular matrices (aECMs) act as crucial barriers, and communicate with the epidermis to trigger protective responses following injury or infection. In Caenorhabditis elegans, the skin aECM, the cuticle, is produced by the epidermis and is decorated with periodic circumferential furrows. We previously showed that mutants lacking cuticle furrows exhibit persistent immune activation (PIA), providing a valuable model to study the link between cuticle damage and immune response. In a genetic suppressor screen, we identified spia-1 as a key gene downstream of furrow collagens and upstream of immune signalling. spia-1 expression oscillates during larval development, peaking between each moult together with patterning cuticular components. It encodes a secreted protein that localises to furrows. SPIA-1 shares a novel cysteine-cradle domain with other aECM proteins. SPIA-1 mediates immune activation in response to furrow loss and is proposed to act as an extracellular signal activator of cuticle damage. This research provides a molecular insight into intricate interplay between cuticle integrity and epidermal immune activation in C. elegans.
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