Mechanisms of tension homeostasis and its role in epithelial morphogenesis
Project/Area Number |
16K18544
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Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Cell biology
|
Research Institution | National Institute for Physiological Sciences |
Principal Investigator |
Otani Tetsuhisa 生理学研究所, 生体機能調節研究領域, 助教 (50415105)
|
Project Period (FY) |
2016-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
Keywords | 密着結合 / 上皮細胞 / 上皮バリア / 上皮極性 / ZO-1 / 上皮管腔構造 / 張力 / 接着結合 / アクチン / ミオシン |
Outline of Final Research Achievements |
Tight Junctions are essential for epithelial barrier formation. In addition to its roles in epithelial barrier, Tight Junctions are thought to regulate epithelial polarity and actomyosin organization, although the detailed molecular mechanisms remained unclear. We have generated ZO-1/ZO-2 double KO cells by genome editing. In ZO-1/ZO-2 double KO cells, Tight Junctions were not formed and epithelial barrier was disrupted. In addition, abnormal accumulation of myosin was observed. Unexpectedly, we found that epithelial polarity was disorganized in ZO-1/ZO-2 deficient cells. Furthermore, ZO-1/ZO-2 deficient cells failed to form polarized cysts when cultured in collagen gel. In contrast, when Adherens Junctions were perturbed, epithelial barrier formation and myosin assembly was not impaired, and epithelial polarity was well developed. These results suggest that ZO-1 and ZO-2 regulate epithelial polarization through Tight Junctions assembly.
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Report
(3 results)
Research Products
(7 results)