Tissue-specific roles of muscle-ECM adhesion in neuromuscular development and maintenance
Official title: Tissue-specific roles for muscle-matrix adhesion in neuromuscular development and homeostasis
Funded at University of Maine Orono · NIH-11406234 · Data updated 2026-11-12
Researchers are studying how muscle-ECM attachments and signaling keep nerves, muscles, and tendons working together in a healthy body, using zebrafish as a model to understand degenerative muscle diseases.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Maine Orono NIH-funded |
| Lab location | 1 site (Orono, United States) |
| Project start | September 5, 2025 |
| Project end | August 31, 2030 |
| Funding year | 2026 |
| Award (this year) | $500,467 |
| NIH project number | 5R01AR084523-02 |
| Project ID | NIH-11406234 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are individuals with neuromuscular conditions linked to glycosylation defects, or healthy volunteers contributing tissue samples or data for translational relevance.
✕Less likely to help
People without neuromuscular conditions affecting NMJ/MTJ function may not directly benefit from this basic mechanistic research.
What this research studies
This project uses a zebrafish model to explore how cells attach muscle to surrounding tissue and how this attachment supports the neuromuscular and myotendinous junctions. The work focuses on the glycosylation of Dystroglycan, a key receptor in the cell-ECM adhesion complex, and how the Dol-P-Man synthase pathway enables this process. By examining how disruptions in these glycosylation steps affect development and maintenance of NMJs and MTJs, the study aims to reveal the basic biology behind neuromuscular diseases. The findings could point toward targets that preserve muscle function and prolong life in patients with glycosylation-related disorders.
Why it matters
Potential benefit: Gaining insight into how muscle-ECM adhesion supports movement could lead to new strategies to treat or slow progression of neuromuscular diseases.
How similar studies have gone: Previous work using animal models has shown that glycosylation defects disrupt NMJ/MTJ integrity, supporting the plausibility of this approach.
Where this research is happening
-
University of Maine Orono
Orono, United States Active
Researchers
- Principal investigator: Henry, Clarissa a — University of Maine Orono
- Study coordinator: Henry, Clarissa a
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.