Duverger Olivier, Morasso Maria I
a Laboratory of Skin Biology, National Institute of Arthritis and Musculoskeletal and Skin Diseases , National Institutes of Health , Bethesda , MD , USA.
Connect Tissue Res. 2018 Dec;59(sup1):30-34. doi: 10.1080/03008207.2017.1408602.
DLX3 is essential for tooth enamel development and is so far the only transcription factor known to be mutated in a syndromic form of amelogenesis imperfecta. Through conditional deletion of Dlx3 in the dental epithelium in mouse, we have previously established the involvement of DLX3 in enamel pH regulation, as well as in controlling the expression of sets of keratins that contribute to enamel rod sheath formation. Here, we show that the decussation pattern of enamel rods was lost in conditional knockout animals, suggesting that DLX3 controls the coordinated migration of ameloblasts during enamel secretion. We further demonstrate that DLX3 regulates the expression of some components of myosin II complexes potentially involved in driving the movement of ameloblasts that leads to enamel rod decussation.
DLX3对牙釉质发育至关重要,并且是迄今为止已知的唯一一种在综合征型牙釉质发育不全中发生突变的转录因子。通过在小鼠牙上皮中条件性缺失Dlx3,我们先前已确定DLX3参与牙釉质pH调节,以及控制有助于牙釉质棱柱鞘形成的角蛋白组的表达。在这里,我们表明在条件性基因敲除动物中牙釉质棱柱的交叉模式消失了,这表明DLX3在牙釉质分泌过程中控制成釉细胞的协调迁移。我们进一步证明,DLX3调节肌球蛋白II复合物某些成分的表达,这些成分可能参与驱动导致牙釉质棱柱交叉的成釉细胞运动。