期刊
DEVELOPMENT
卷 146, 期 15, 页码 -出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dev.170241
关键词
FGF; Notch; Craniofacial development; Enthesis; Perichondrium; Tendon; Mouse
资金
- National Institutes of Health [1R01DE025222, R01 DE025222-01S1, T90DE021982]
- March of Dimes Foundation [36-FY15-233]
- Shriners Hospitals for Children [85410-POR-14]
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [T90DE021982, R01DE025222] Funding Source: NIH RePORTER
Tendon and bone are attached by a transitional connective tissue that is morphologically graded from tendinous to osseous and develops from bipotent progenitors that co-express scleraxis (Scx) and Sox9 (Scx(+)/Sox9(+)). Scx(+)/Sox9(+) progenitors have the potential to differentiate into either tenocytes or chondrocytes, yet the developmental mechanism that spatially resolves their bipotency at the tendon-bone interface during embryogenesis remains unknown. Here, we demonstrate that development of Scx/Sox9(+) progenitors within the mammalian lower jaw requires FGF signaling. We find that loss of Fgfr2 in the mouse tendon-bone interface reduces Scx expression in Scx(+)/Sox9(+) progenitors and induces their biased differentiation into Sox9(+) chondrocytes. This expansion of Sox9(+) chondrocytes, which is concomitant with decreased Notch2-DII1 signaling, prevents formation of a mixed population of chondrocytes and tenocytes, and instead results in ectopic endochondral bone at tendon-bone attachment units. Our work shows that FGF signaling directs zonal patterning at the boundary between tendon and bone by regulating cell fate decisions through a mechanism that employs Notch signaling.
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