Project/Area Number |
06454140
|
Research Category |
Grant-in-Aid for General Scientific Research (B)
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Allocation Type | Single-year Grants |
Research Field |
General anatomy (including Histology/Embryology)
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Research Institution | KYOTO UNIVERSITY |
Principal Investigator |
SHIOTA Kohei Kyoto Univ., Fac.of Med.Professor, 医学研究科, 教授 (80109529)
|
Co-Investigator(Kenkyū-buntansha) |
TAKIGAWA Toshiya Kyoto Univ., Fac.of Med.Instructor, 医学研究科, 助手 (90263095)
ISHIBASHI Makoto Kyoto Univ., Fac.of Med.Instructor, 医学研究科, 助手 (30232341)
MORI Chisato Kyoto Univ., Fac.of Med.Associste Professor, 医学研究科, 助教授 (90174375)
|
Project Period (FY) |
1994 – 1995
|
Project Status |
Completed (Fiscal Year 1995)
|
Budget Amount *help |
¥7,300,000 (Direct Cost: ¥7,300,000)
Fiscal Year 1995: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1994: ¥5,500,000 (Direct Cost: ¥5,500,000)
|
Keywords | Apoptsis / Programd cell death / DNA fragmentation / morphogenesis / palate / limb / mouse fetus / Abnormal Development |
Research Abstract |
Programd cell death is a common event during mammalian morphogenesis, which is morphologically known as apoptosis. The cell death in interdigital spaces of the mammalian developing limb and the disappearance of the midline epithelial seam during the fusion process of the mammalian secondary palate are classical examples of morphogenetic programd cell death. For the formation of various structures during development, programd cell death has been considered to play a key role by eliminating unnecessary cells to achieve complicated histogenesis and organogenesis. However, our studies showed that programd cell death in the mammalian limb and palate development plays more aggressive roles in addition to the elimination of unnecessary cells. In mammalian limb development, programd cell death may play a role in preventing the formation of extra digits and reducing the size of the first digit as well as in the digit separation and joint formation (Mori et al., 1995 ; Mori, 1995). In the proces of palate fusion, programd cell death may be reguired for the midline epithelial seam to disrupt or for elimination of unnecessary cells which can not migrate or transform, but may not be necessary for initial contact of palatal shelves or for the epithelial fusion of opposing palatal shelves (Mori et al., 1994). In addition, we reported the morphological analysis of limb malformations induced by BrdU in fetal mice (Nakamura et al., 1995) and the altered expression of Hoxd-11 gene transcripts at the anterior region of the hindlimb bud in the formation of preaxial polydactyly and triphalangism of the first digit in BrdU-treated mouse fetuses (Nakamura et al., 1996). Moreover, we developed the antisense strategy in organ culture of fetal mouse palates for analysis of morphogenetic mechnisms (Naitoh et al., 1996).
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