Involvement of calcium signal in gene regulation related to drug exhaust
| Project/Area Number |
25460128
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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 |
Natural medicines
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| Research Institution | Osaka City University |
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Principal Investigator |
FUJITA Ken-ichi 大阪市立大学, 大学院理学研究科, 准教授 (10285281)
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| Co-Investigator(Kenkyū-buntansha) |
USUKI Yoshinosuke 大阪市立大学, 大学院理学研究科, 准教授 (30244651)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 薬剤耐性 / カルシウムシグナル / アネトール / 出芽酵母 / 抗真菌作用 / SWI/SNF複合体 / ゴルジ体Ca2+-ATPase / カルシウム代謝異常 / anethole / drug resistance / antifungal / PDR5 / PMR1 / LGE1 / ABCトランスポーター / 細胞内カルシウム調節 / フェニルプロパノイド / 真菌 |
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| Outline of Final Research Achievements |
Anethole expresses synergistic antifungal activity via restriction of over-expression of drug exhaust pump PDR5 and its transcription factor PDR3. We found that the restriction was involved in the restriction of PDR5 and PDR3 over-expression induced by LGE1, which is over-expressed as a result of deprivation of mitochondrial DNA. In addition, the synergy disappeared in strains lacking PMR1 and genes related to chromatin remodeling complexes SWI/SNF. Whereas anethole accelerated Ca2+ accumulation, drug exhaust was constitutively restricted in the strain described above. Therefore, these results indicated that regulatory mechanism of Ca2+ homeostasis was involved in regulation of genes related to drug exhaust and elevation of Ca2+ levels was provably secondary effects on the gene regulation.
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Report
(4 results)
Research Products
(14 results)
