| 研究課題/領域番号 |
19F19781
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| 研究機関 | 国立研究開発法人理化学研究所 |
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研究代表者 |
杉本 慶子 国立研究開発法人理化学研究所, 環境資源科学研究センター, チームリーダー (30455349)
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| 研究分担者 |
FAVERO DAVID 国立研究開発法人理化学研究所, 環境資源科学研究センター, 外国人特別研究員
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| 研究期間 (年度) |
2019-11-08 – 2022-03-31
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| キーワード | AHL / SOB3 / petiole / PIF / transcription / growth / plants / photomorphogenesis |
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| 研究実績の概要 |
The AHL transcription factors are known to repress hypocotyl growth in seedlings. However, it is largely unknown how AHLs are positioned in the gene regulatory networks (GRNs) which regulate growth. I have sought to begin to answer this question by studying how AHLs regulate petiole growth in Arabidopsis. Genetic studies combined with data from RNA-seq and ChIP-seq experiments have revealed that SOB3/AHL29 and other AHLs repress petiole elongation by inhibiting the ability of PHYTOCHROME INTERACTING FACTORs (PIFs) to activate the transcription of growth-promoting genes. This led me to investigate in detail the mechanism by which SOB3 inhibits PIF-mediated activation of growth-promoting genes. Semi-quantitative western blot analysis revealed that induction of SOB3 reduces PIF4 protein levels. ChIP-qPCR further revealed PIF4 binding to target growth-promoting genes is reduced following SOB3 induction.
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| 現在までの達成度 (区分) |
現在までの達成度 (区分)
2: おおむね順調に進展している
理由
Within the last fiscal year of this project, the western blot and ChIP-qPCR experiments described above were completed. These were the final pieces of data needed to finish a paper that was resubmitted to Current Biology and then published online in this journal in March. Specifically, this paper describes how AHLs repress petiole growth by reducing PIF-mediated activation of growth-promoting genes in two different ways. First, AHLs reduce the level of PIF4 protein, likely by enhancing its degradation, as PIFs are relatively unstable in light-grown plants. Second, AHLs bind similar DNA regions as those bound by PIFs, directly inhibiting the ability of these transcription factors to bind to and activate target genes.
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| 今後の研究の推進方策 |
Several different studies suggest that AHLs regulate gene transcription by serving as part of a larger DNA-protein complex. Some putative co-factors potentially important for AHL function have been identified. In order to further investigate how AHLs fit into GRNs that regulate growth, I will evaluate how these putative co-factors affect AHL-mediated transcriptional changes and growth repression. Further, I will investigate how various stimuli and transcription factors regulate expression of AHLs.
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