Journal
DEVELOPMENT
Volume 146, Issue 20, Pages -Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dev.182782
Keywords
Tendon development; Musculoskeletal; Scleraxis; Mouse
Categories
Funding
- National Institutes of Health/National Institute of Arthritis and Musculoskeletal and Skin Diseases [R01AR055640, R01AR055973, R01DC008595]
- Shriners Hospitals for Children [85410-POR-14]
- Arthritis Foundation
Ask authors/readers for more resources
The transcription factor scleraxis (Scx) is required for tendon development; however, the function of Scx is not fully understood. Although Scx is expressed by all tendon progenitors and cells, only long tendons are disrupted in the Scx(-/-) mutant; short tendons appear normal and the ability of muscle to attach to skeleton is not affected. We recently demonstrated that long tendons are formed in two stages: first, by muscle anchoring to skeleton via a short tendon anlage; and second, by rapid elongation of the tendon in parallel with skeletal growth. Through lineage tracing, we extend these observations to all long tendons and show that tendon elongation is fueled by recruitment of new mesenchymal progenitors. Conditional loss of Scx in mesenchymal progenitors did not affect the first stage of anchoring; however, new cells were not recruited during elongation and long tendon formation was impaired. Interestingly, for tenocyte recruitment, Scx expression was required only in the recruited cells and not in the recruiting tendon. The phenotype of Scx mutants can thus be understood as a failure of tendon cell recruitment during tendon elongation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available