在细菌感染中,SIRT2依赖的素H3K18脱乙的作用
Haig A Eskandarian1, Francis Impens, Marie-Anne Nahori
1Unité des Interactions Bactéries-Cellules, Institut Pasteur, Paris, France.
概括
病原性细菌通过劫持脱乙酶二素 (SIRT2) 来重新编程宿主细胞. 这种表观遗传机制涉及SIRT2介导的基因素脱甲基化,这对于细菌感染的成功至关重要.
科学领域:
- 微生物学 微生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 分子生物学分子生物学
背景情况:
- 病原体在感染期间操纵宿主细胞转录.
- 病原体诱导的转录变化背后的机制往往不清楚.
研究的目的:
- 为了阐明宿主脱乙酶Sirtuin 2 (SIRT2) 在Listeria monocytogenes感染中的作用.
- 研究病原体用来改变宿主转录的表观遗传机制.
主要方法:
- 研究了在Listeria monocytogenes感染期间SIRT2转移到细胞核的过程.
- 研究了SIRT2与基因转录起点的关联.
- 分析的素H3氨酸18 (H3K18) 脱乙烯化.
- 使用SIRT2活动抑制和SIRT2淘汰 (SIRT2-/-) 鼠标模型.
主要成果:
- 一种Listeria monocytogenes感染会触发SIRT2的核转位,这取决于细菌因子InlB.
- SIRT2与感染期间被抑制的基因的转录起点相关.
- 在lysine 18 (H3K18) 上,SIRT2 脱乙化基素 H3.
- 阻断SIRT2活动或使用SIRT2-/-小鼠显著损害了细菌感染.
结论:
- 在Listeria monocytogenes感染中,SIRT2介导的H3K18脱甲基化是至关重要的.
- 致病细菌利用SIRT2的表观遗传重编程来控制宿主细胞.
- 这项研究揭示了一种由病原体施加的新型表观遗传机制.
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