| 研究課題/領域番号 |
21K15066
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| 研究機関 | 京都大学 |
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研究代表者 |
CHEN Xun 京都大学, 高等研究院, 特定助教 (30885158)
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| 研究期間 (年度) |
2021-04-01 – 2024-03-31
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| キーワード | pathogen-specific / transposable elements / immune cells / transcriptome / evolution |
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| 研究実績の概要 |
We have identified transposable elements (TEs) that are induced by salmonella but not by influenza virus infection in human macrophages last year. We further collected available RNA-seq datasets in immune cells following different pathogen infection separately.
This year, We further identified 34 TE families that are highly activated following ebolavirus infection and 43 TE families are activated following influenza infection. They were consistently highly activated in multiple immune cells compared to other pathogens. We also found that these pathogen-specific families are mostly integrated before primates during evolution.
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| 現在までの達成度 (区分) |
現在までの達成度 (区分)
3: やや遅れている
理由
After we found the pathogen-specific TE families, we are particulally interested in these differentially activated TEs upon pathogen infection.
We have carefully examine the TE families we found in multiple immune cells.
We have also found that these families are shared between primates while some of them are absent in mouse genome.
We then want to look at whether these TE families shape the evolution of the immune response to different pathogens by epigenetically regulating their ajacent immune-related genes.
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| 今後の研究の推進方策 |
To achieve our goals, we have purchased the human macrophage cell line THP-1 for the planed epigenetic profiles to functinonally validate the regulation of activated endogenous retrovirus families.
We also plan to use the Massively Parallel Reporter Assay to validate the regulatory activity of these families in THP-1 cell line following different pathogen infection.
We will also compare the results in THP-1 cell line with human primary macrophages to examine their functionality in primary cells.
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| 次年度使用額が生じた理由 |
As we planned, we will perform additional RNA-seq, ATAC-seq, and Chip-seq sequencing experiment of the THP-1 cell line following infection in this year.
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