TGF-β Signaling in Cranial Neural Crest Affects Late-Stage Mandibular Bone Resorption and Length
Posted on: 7 August 2024
Preprint posted on 24 May 2024
Categories: cell biology, developmental biology, molecular biology
Background
This preprint investigates the role of TGF-β signaling in neural crest mesenchyme (NCM)-derived osteoblast lineage cells in lower jaw (mandible) development. Previous reports show that these cells influence mandibular development by regulating osteoclast formation and bone resorption. The loss of TGFBR1 in NCM leads to micrognathia a condition in which the lower jaw is undeveloped. Despite significant craniofacial defects, mice lacking Tgfbr1 in NCM showed similar mandibular bone quality, mineral density, and resorption patterns as healthy controls in the current study. However, histological analysis revealed fewer osteoclasts and decreased expression of the osteoclast-related gene Rank. No significant differences were found in Rankl, Opg, and M-csf expression, suggesting other NCM-derived factors mediate the observed changes.
The current study confirms known mandibular defects in Tgfbr1fl/fl;Wnt1-Cre mice and reveals decreased osteoclast numbers and related gene expression without changes in Rankl, Opg, or M-csf. Further research into TGFBR1 signaling and its role in osteoclast regulation by NCM-derived osteoblasts is crucial for understanding mandibular development and developing treatments for related disorders such as Loeys-Dietz Syndrome I.
Key contributions
The authors of this preprint reveal the contribution of TGFBR1 in mandible development. They managed to do so by using the Cre system in mice and inhibition studies in quail embryo.
1. Tgfbr1fl/fl; Wnt1-Cre embryos at E18.5 exhibited severe micrognathia and lacked the condylar, coronoid, and angular processes, consistent with previous findings. These embryos also had severe, perinatal lethal craniofacial defects.
2. Micro-CT imaging between E16.5 and E18.5 revealed significant morphological differences and a substantial decrease in bone volume in Tgfbr1fl/fl;Wnt1-Cre mandibles compared to controls.
3. Inhibition of TGFBR1 at a specific developmental stage in quail embryos resulted in shorter lower jaws, mirroring the micrognathia observed in Tgfbr1fl/fl;Wnt1-Cre mice. That indicates that TGF-β signaling in neural crest cells influences mandibular bone resorption and osteoclast activity, but not through major changes in Rankl, Opg, or M-csf expression.
These findings indicate that TGF-β signaling in neural crest cells does not significantly affect mandibular bone quality, even though it leads to severe morphological defects.
Questions/Future directions
1. In this study, the TGFBR1 hasn’t shown any significant contribution to mandibular formation. Have you tried checking the other receptor types and the SMADs that play an important role in TGF-beta signaling?
2. Despite the decrease in osteoclast number, there is no significant effect on the morphology of the mandibles of Tgfbrf1/f1; Wnt1-cre mice. Is there a feedback mechanism or pathway that has no impact on the overall morphology of the mandibles?
doi: https://doi.org/10.1242/prelights.38020
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