Protogenin, a new member of the immunoglobulin superfamily, is implicated in the development of the mouse lower first molar

BMC Developmental Biology. 2010;10(1):115 DOI 10.1186/1471-213X-10-115

 

Journal Homepage

Journal Title: BMC Developmental Biology

ISSN: 1471-213X (Online)

Publisher: BMC

LCC Subject Category: Science: Biology (General)

Country of publisher: United Kingdom

Language of fulltext: English

Full-text formats available: PDF, HTML

 

AUTHORS

Wada Hiroko
Nagata Kengo
Ookuma Yukiko
Fujiwara Hiroaki
Yamaza Haruyoshi
Xie Ming
Kobayashi Ieyoshi
Kiyoshima Tamotsu
Takahashi Keiko F
Sakai Takako
Terada Yoshihiro
Sakai Hidetaka

EDITORIAL INFORMATION

Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 20 weeks

 

Abstract | Full Text

<p>Abstract</p> <p>Background</p> <p><it>Protogenin (Prtg) </it>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.</p> <p>Results</p> <p>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 <it>Prtg </it>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.</p> <p>Conclusion</p> <p>These results indicated that the <it>Prtg </it>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.</p>