ArticlePloS one2018
Trynity controls epidermal barrier function and respiratory tube maturation in Drosophila by modulating apical extracellular matrix nano-patterning.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Mechanical control of the insect extracellular matrix nanostructure.Science advances · 2026Article
- Apical cell expansion maintained by Dusky-like establishes a scaffold for corneal lens morphogenesis.Science advances · 2024Article
- Improving Polysaccharide-Based Chitin/Chitosan-Aerogel Materials by Learning from Genetics and Molecular Biology.Materials (Basel, Switzerland) · 2022Review
- Crosstalk between basal extracellular matrix adhesion and building of apical architecture during morphogenesis.Biology open · 2021Review
- High-precision targeting workflow for volume electron microscopy.The Journal of cell biology · 2021Article
- Glycosylhydrolase genes control respiratory tubes sizes and airway stability.Scientific reports · 2020Article
- Form and function of the apical extracellular matrix: new insights fromFaculty reviews · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The outer surface of insects is covered by the cuticle, which is derived from the apical extracellular matrix (aECM). The aECM is secreted by epidermal cells during embryogenesis. The aECM exhibits large variations in structure, function, and constituent molecules, reflecting the enormous diversity in insect appearances. To investigate the molecular principles of aECM organization and function, here we studied the role of a conserved aECM protein, the ZP domain protein Trynity, in Drosophila melanogaster. We first identified trynity as an essential gene for epidermal barrier function. trynity mutation caused disintegration of the outermost envelope layer of the cuticle, resulting in small-molecule leakage and in growth and molting defects. In addition, the tracheal tubules of trynity mutants showed defects in pore-like structures of the cuticle, and the mutant tracheal cells failed to absorb luminal proteins and liquid. Our findings indicated that trynity plays essential roles in organizing nano-level structures in the envelope layer of the cuticle that both restrict molecular trafficking through the epidermis and promote the massive absorption pulse in the trachea.
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Registered trials
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