Protogenin, a new member of the immunoglobulin superfamily, is implicated in the development of the mouse lower first molar.
Protogenin, a new member of the immunoglobulin superfamily, is implicated in the development of the mouse lower first molar.
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原蛋白是免疫球蛋白超家族的新成员，与小鼠下部磨牙的发展有关。
DOI：
10.1186/1471-213x-10-115
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发表时间：
2010-11-25
影响因子：
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通讯作者：
Sakai H
中科院分区：
文献类型：
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作者：
Takahashi KF;Kiyoshima T;Kobayashi I;Xie M;Yamaza H;Fujiwara H;Ookuma Y;Nagata K;Wada H;Sakai T;Terada Y;Sakai H
原基因(Protogenin，PRTG)是小鼠胚胎第10.5天(E10.5天)下颌骨中高表达的基因，通过对胚胎第10.5天和第12.0天的下颌骨进行基因消减，发现PRTG基因在小鼠下颌骨中高表达。PRTG是缺失的结直肠癌(DCC)家族的新成员，由DCC、新生素、PUNC和NOPE组成。虽然这些成员在胚胎中枢神经系统的发育中发挥了重要作用，但最近的研究也集中在非神经元组织上。然而，关于胎儿对PRTG的非神经元组织的需求以及这可能如何与牙胚发育相关的知识很少。本研究探讨了PRTG在小鼠下颌第一磨牙牙胚发育过程中的功能意义。在器官发生的早期，PTRG优先表达。胚胎10.5天，下颌骨间充质细胞广泛表达PRTG基因和蛋白。口腔上皮细胞PRTG也呈阳性反应。E12.0后PRTG在下颌骨间充质细胞中的表达强度明显降低，且仅限于牙芽形成的部位。在牙胚的上皮细胞中也观察到了信号。E16.0和E18.0的内釉上皮细胞内可见弱信号。用日本血凝病毒-含PrTGODN的脂质体(AS-S-antisense-phosphorothioated-oligodeoxynucleotide)在E10.5培养的下颌骨中的抑制实验表明，对牙胚的生长有明显的抑制作用。研究了PRTG与小鼠E10.5下颌骨成牙相关基因表达的关系，证实PRTG AS-S-ODN作用24小时后，小鼠E10.5下颌骨中BMP-4的表达显著降低。提示PRTG可能与牙胚的初始形态发生有关，导致小鼠下第一磨牙内釉上皮细胞的分化。因此，更好地了解PRTG的功能可能对揭示牙胚发育的宝贵机制起到关键作用。
Protogenin (Prtg) has been identified as a gene which is highly expressed in the mouse mandible at embryonic day 10.5 (E10.5) by a cDNA subtraction method between mandibles at E10.5 and E12.0. Prtg is a new member of the deleted in colorectal carcinoma (DCC) family, which is composed of DCC, Neogenin, Punc and Nope. Although these members play an important role in the development of the embryonic central nervous system, recent research has also shed on the non-neuronal organization. However, very little is known regarding the fetal requirement of the non-neuronal organization for Prtg and how this may be associated with the tooth germ development. This study examined the functional implications of Prtg in the developing tooth germ of the mouse lower first molar. Ptrg is preferentially expressed in the early stage of organogenesis. Prtg mRNA and protein were widely expressed in the mesenchymal cells in the mandible at E10.5. The oral epithelial cells were also positive for Prtg. The expression intensity of Prtg after E12.0 was markedly reduced in the mesenchymal cells of the mandible, and was restricted to the area where the tooth bud was likely to be formed. Signals were also observed in the epithelial cells of the tooth germ. Weak signals were observed in the inner enamel epithelial cells at E16.0 and E18.0. An inhibition assay using a hemagglutinating virus of Japan-liposome containing Prtg antisense-phosphorothioated-oligodeoxynucleotide (AS-S-ODN) in cultured mandibles at E10.5 showed a significant growth inhibition in the tooth germ. The relationship between Prtg and the odontogenesis-related genes was examined in mouse E10.5 mandible, and we verified that the Bmp-4 expression had significantly been decreased in the mouse E10.5 mandible 24 hr after treatment with Prtg AS-S-ODN. These results indicated that the Prtg might be related to the initial morphogenesis of the tooth germ leading to the differentiation of the inner enamel epithelial cells in the mouse lower first molar. A better understanding of the Prtg function might thus play a critical role in revealing a precious mechanism in tooth germ development.