Analysis of mechanism of anorectal development in new anorectalmalformations model mice.
| Project/Area Number |
22791711
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatric surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
LEE Kwang-jong 熊本大学, 医学部附属病院, 助教 (00467995)
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| Co-Investigator(Renkei-kenkyūsha) |
SUDA Hiroko 熊本大学, 医学部附属病院, 助教 (40632659)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2011: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2010: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
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| Keywords | 発生 / 分化 / 解剖学 / 発生・分化 / シグナル伝達 |
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| Research Abstract |
BACKGROUND AND AIMS: Danforth's short tail (Sd) mutant mice showanorectal malformations (ARMs). In our previous study, the co-presence of Skt (Gt)mutation increased the incidence of ARMs in Sd mutant to 100%. Our aims in this studyare determining the Skt expression around the cloaca during the anorectal developmentand demonstrating the role of Skt gene in ARMs. METHODS: Embryos, normal controls [+Skt(Gt)/+Skt (Gt)] and ARMs models [Sd Skt (Gt)/+Skt (Gt)], from embryonic day (E)9.5 to E12.5, were evaluated with X-gal staining. RESULTS: In [Sd Skt (Gt)/+Skt (Gt)]mutant embryos, the cloacal plates failed to extend proximodistally and, consequently,the dorsal part of cloacal plate was defective at E11.5. Skt expressing cells were detectedin the shortened cloacal plate and in the thickened mesenchyme dorsal to it. CONCLUSIONS:We showed the spatial and temporal expression of Skt gene in the cloacal plate formation.
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Report
(4 results)
Research Products
(11 results)
