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Publication

Altered bone growth dynamics prefigure craniosynostosis in a zebrafish model of Saethre-Chotzen syndrome.

eLife | 2018

Cranial sutures separate the skull bones and house stem cells for bone growth and repair. In Saethre-Chotzen syndrome, mutations in TCF12 or TWIST1 ablate a specific suture, the coronal. This suture forms at a neural-crest/mesoderm interface in mammals and a mesoderm/mesoderm interface in zebrafish. Despite this difference, we show that combinatorial loss of TCF12 and TWIST1 homologs in zebrafish also results in specific loss of the coronal suture. Sequential bone staining reveals an initial, directional acceleration of bone production in the mutant skull, with subsequent localized stalling of bone growth prefiguring coronal suture loss. Mouse genetics further reveal requirements for Twist1 and Tcf12 in both the frontal and parietal bones for suture patency, and to maintain putative progenitors in the coronal region. These findings reveal conservation of coronal suture formation despite evolutionary shifts in embryonic origins, and suggest that the coronal suture might be especially susceptible to imbalances in progenitor maintenance and osteoblast differentiation.

Pubmed ID: 30375332 RIS Download

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Associated grants

Agency: NIDCR NIH HHS, United States
Id: T90DE021982
Agency: NIDCR NIH HHS, United States
Id: R35DE027550
Agency: NIDCR NIH HHS, United States
Id: R01 DE026339
Agency: NIDCR NIH HHS, United States
Id: R35 DE027550
Agency: NIDCR NIH HHS, United States
Id: T90 DE021982
Agency: NIDCR NIH HHS, United States
Id: R01DE026339
Agency: NIDCR NIH HHS, United States
Id: F31DE024031
Agency: NIDCR NIH HHS, United States
Id: F31 DE024031

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Fiji (tool)

RRID:SCR_002285

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RRID:SCR_007353

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Imaris (tool)

RRID:SCR_007370

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