| Project/Area Number |
16K21272
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
General physiology
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| Research Institution | Yokohama City University |
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Principal Investigator |
Goulas Spyros 横浜市立大学, 医学研究科, 特任助教 (90644352)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | Cell Polarity / Epithelial Homeostasis / Cell Death / Barrier Malfunction / Overproliferation / 上皮恒常性 / 細胞極性 / 上皮機能 |
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| Outline of Final Research Achievements |
To understand how epithelia maintain homeostasis, in FY2016 I have screened knockdown lines using a candidate approach of known cell polarity regulators in MDCK cells. I have identified and verified several candidates that resulted in phenotypes during epithelial homeostasis. Some of the phenotypes observed included overproliferation, excessive cell death and epithelial barrier malfunction.
In FY2017, I characterized the candidates identified from the knockdown screen of cell polarity regulators during epithelial homeostasis. I identified a group of genes that resulted in defects at cell-cell contact sites specifically during cell death. Interestingly, this was accompanied by a transient increases in the integrity of the epithelium. I was able to identify the downstream molecular targets, thereby giving insights into the molecular mechanism of how epithelia maintain barrier function during during homeostasis.
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