Sox2 controls asymmetric patterning of ameloblast lineage commitment by regulation of FGF signaling in the mouse incisor

AbstractMouse incisors are covered by enamel only on the labial side and the lingual side is covered by dentin without enamel. This asymmetric distribution of enamel makes it possible to be abrased on the lingual side, generating the sharp cutting edge of incisor on the labial side. The abrasion of mouse incisors is compensated by the continuous growth throughout life. Epithelium stem cells responsible for its continuous growth are reported to localize within the labial cervical loop. The transcription factorSox2 plays important roles in the maintenance of stem cell pluripotency and organ formation. We previously found thatSox2mainly expressed in the dental epithelium. Besides,Sox2 has been reported to be a dental epithelium stem cell marker in the incisor. However, the exact mechanism ofSox2 controlling amelogenesis is still not quite clearly elucidated. Here we report that conditional deletion ofSox2 in the dental epithelium usingShhcre caused impaired ameloblast differentiation in the labial side and induced ectopic ameloblast-like cell differentiation on the lingual side. AbnormalFGF gene expression was detected by RNAscope in situ hybridization in the mutant incisor. Collectively, we speculate that asymmetric ameloblast lineage commitment of mouse incisor might be regulated bySox2 throughFGF signaling.
Source: Journal of Molecular Histology - Category: Laboratory Medicine Source Type: research