2009 Fiscal Year Final Research Report
Making conditional knockout mouse of the gene coding inversin and the significance of inversion in the cilia-dependent renal disease
| Project/Area Number |
19590965
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
TSUCHIYA Ken Tokyo Women's Medical University, 医学部, 准教授 (00246472)
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| Co-Investigator(Renkei-kenkyūsha) |
YOSHIDA Takumi 東京女子医科大学, 医学部, 助教 (80297449)
TSUCHIYA Mariko 東京女子医科大学, 医学部, 准教授 (00266826)
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| Project Period (FY) |
2007 – 2009
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| Keywords | siRNA / 左右軸 / ノックアウトマウス / 繊毛 / 嚢胞腎 / inv遺伝子 |
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| Research Abstract |
Vertebrate organisms have a common left-right asymmetry of their visceral organs. However, all unpaired organs of the chest and abdomen, such as heart, stomach, spleen and liver, develop from the midline in the fetus and localize to their normal positions in the adult. The phenotype of the inv mouse is a consistent mirror-image reversal of the left-right polarity (situs inversus) and cystic formation of the kidneys. In this study, the targeting vector of the inversion of embryonic turning (inv) for conditional knockout mounting interferon-induced promoter was constructed. Genomic southern hybridization indicated that these gene spans the whole deleted region, implying that the homozygous inv mice have intragenic deletion of this gene. We also analyzed the physiologic and pathophysiological findings of mice and renal tubular cells kidney associated with an inversion of embryonic turning. The results suggested that there might be a possibility that a cytoskeletal abnormality was involved in the mechanism and production of both structural abnormalities, inversion and cyst formation in the kidney.
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