2011年5月
The canonical Wnt signaling pathway is not involved in renal cyst development in the kidneys of inv mutant mice
KIDNEY INTERNATIONAL
- ,
- ,
- ,
- 巻
- 79
- 号
- 9
- 開始ページ
- 957
- 終了ページ
- 965
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1038/ki.2010.534
- 出版者・発行元
- NATURE PUBLISHING GROUP
Recent studies have identified several genes whose defects cause hereditary renal cystic diseases with most of the gene products located in the primary cilia. It has been suggested that primary cilia are involved in signaling pathways, defects of which result in abnormal cell proliferation and randomization of oriented cell division in the kidney leading to cyst formation. Mice with a mutation in the inv gene are a model for human nephronophthisis type 2 and develop multiple renal cysts. Inv protein (also called inversin) is located in the base of primary cilia and acts as a switch from canonical to non-canonical Wnt signaling. Here, we studied the orientation of cell division and proliferation in the kidneys of inv mutant mice, as its loss is thought to maintain activation of the canonical Wnt signaling. To establish if canonical signaling was involved in this process, we mated inv mutant with BATlacZ mice to measure canonical Wnt activity. Based on these reporter mice, nuclear localization and phosphorylation of beta-catenin, and responsiveness to Wnt ligands in inv mutant cells, we found that random oriented cell division is an initial event for renal tubule expansion and precedes cell proliferation. Thus, our results do not support the hypothesis that canonical Wnt signaling causes renal cyst development in these mice. Kidney International (2011) 79, 957-965; doi:10.1038/ki.2010.534; published online 19 January 2011
- リンク情報
- ID情報
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- DOI : 10.1038/ki.2010.534
- ISSN : 0085-2538
- PubMed ID : 21248711
- Web of Science ID : WOS:000289514400005