Molecular mechanisms of mechanical signal sensing by motile cilia in vertebrate organogenesis

• Project/Area Number: 23657141
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Developmental biology
• Research Institution: Shumei University (2013); The University of Tokyo (2011-2012)
• Principal Investigator: KOSHIDA Sumito 秀明大学, 人文社会・教育科学系, 教授 (40342638)
• Project Period (FY): 2011 – 2012
• Project Status: Completed (Fiscal Year 2013)
• Budget Amount: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000); Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000); Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
• Keywords: 細胞・組織 / 発生・分化 / シグナル伝達

Research Abstract

Polycystic kidney disease (PKD) is a serious congenital disease in vertebrates, in which epithelial cells in renal tubules abnormally proliferate and become flattened in shape leading to development of numerous cysts in the entire kidney.
In this study, we analyzed the medaka mutant kintoun (ktu) that develops PKD. We revealed that renal epithelial cells of ktu mutant were flattened before beginning of urine flow. Cell transplantation experiments showed that ktu seemed to cause this morphological change in a cell-autonomous manner. To further understand the function of Ktu, we identified Ktu-interacting proteins and analyzed the roles of these proteins, especially in the developmental events requiring motile cilia in zebrafish.