| Project/Area Number |
17K07385
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cell biology
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| Research Institution | Kyoto Institute of Technology |
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Principal Investigator |
Yoshida Hideki 京都工芸繊維大学, 応用生物学系, 准教授 (30570600)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2017: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | ショウジョウバエ / yki / mRNA局在化 / yki mRNA / 翻訳抑制 / P-body / mRNA細胞内局在 / yorkie mRNA / P-bodies |
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| Outline of Final Research Achievements |
We biologically identified 13 proteins, including two aminoacyl tRNA synthetases (ARS), which are purified with the 3’ untranslated region of yki mRNA by using a mass spectrometer. Therefore, we investigated whether yki genetically interact with other tRNA synthetases. As a result, we found at least 14 ARSs were genetically interacting with yki and showed a loss of pigmentation or the ectopic melanization especially in the posterior region, which are not typical phenotypes derived from yki overexpression. Because we found that the amount of Yki protein in ARS knockdown cells was increased, we will investigate whether the amount of Yki protein in ARS knockdown flies is also increased.
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| Academic Significance and Societal Importance of the Research Achievements |
yki遺伝子の哺乳類相同遺伝子はYAPであり、様々ながんで高発現するがん遺伝子である。YkiやYAPは、がん抑制経路Hippo経路を介して、リン酸化により抑制的に制御される。このリン酸化部位に変異をもつYkiやYAPの過剰発現は、がん化を誘導することから、リン酸化の制御の重要性が注目されてきた。しかし、一方で、がん患者のYAPのリン酸化部位に変異は見つかっておらず、またYAPタンパク質の高発現の原因も明らかになっていない。今回、我々は、ARSとykiが遺伝学的に相互作用すること、ARSノックダウンによりYkiタンパク質が増加することを見出し、がん化メカニズムの解明に迫る可能性を示した。
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