Mechanism of reduced fecundity due to obesity
Project/Area Number |
18K06351
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 45010:Genetics-related
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Research Institution | Okayama University |
Principal Investigator |
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Project Period (FY) |
2018-04-01 – 2022-03-31
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Project Status |
Completed (Fiscal Year 2021)
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Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2021: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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Keywords | ショウジョウバエ / 妊性 / 精液 / 栄養シグナル / ストレス応答 / ステロイドホルモン |
Outline of Final Research Achievements |
The male reproductive organ accessory gland in Drosophila produces components of seminal fluid. Excess nutrient signaling reduces fecundity through changes in gene expression that are mediated by inhibition of degradation of the transcriptional regulator Dve. Microarray analysis identified Dve target gene candidates. In addition, a novel feedback mechanism is proposed that the strong stress induces accumulation of Dve proteins and suppresses the expression of the initial stress response genes (molecular chaperon, ER stress sensor Xbp1).
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Academic Significance and Societal Importance of the Research Achievements |
過剰栄養ストレスが妊性低下を招く原因として精液成分の変化が大きく影響していることを示し,精液成分を変化させる経路において介在する候補遺伝子群を同定することができた.
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Report
(5 results)
Research Products
(14 results)
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[Journal Article] Nutrient conditions sensed by the reproductive organ during development optimize male fecundity in Drosophila2018
Author(s)
Kubo, A., Matsuka, M., Minami, R., Kimura, F., Sakata-Niitsu, R., Kokuryo, A., Taniguchi, K., Adachi-Yamada, T., Nakagoshi, H.
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Journal Title
Genes to Cells
Volume: 23
Issue: 7
Pages: 557-567
DOI
Related Report
Peer Reviewed / Open Access
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