Nature子刊:菌群通过改变DNA甲基化以调控肠道稳态及炎症
创作:szx 审核:szx 03月01日
  • 分离正常小鼠及无菌小鼠的结肠隐窝中的肠道上皮细胞(IEC),对IEC中的mRNA转录组及DNA甲基化进行对比分析;
  • 肠道菌群改变IEC中多个基因的表达,824个基因上调(多与有丝分裂相关),358个基因下调(多与细胞外基质及代谢过程相关);
  • 肠道菌群改变IEC中的DNA甲基化,12983个低甲基化区域(LMR)的甲基化水平降低,3115个LMR的甲基化水平升高;
  • 在正常小鼠中低甲基化且高表达的300个基因中,多为维持肠道稳态的“哨兵炎症基因”。
主编推荐语
szx
Nature Microbiology上发表的一项最新研究,对比分析了正常小鼠及无菌小鼠的肠道上皮细胞中的基因表达及DNA甲基化谱,鉴定出了因暴露于肠道菌群而发生表达变化或DNA甲基化变化的基因,并发现菌群的存在促进了一些维持肠道稳态的“哨兵炎症基因”(sentinel inflammatory genes)的去甲基化以增强其表达,提示菌群可通过调节表观遗传组以维持肠道稳态。
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The microbiota programs DNA methylation to control intestinal homeostasis and inflammation

菌群调节DNA甲基化以调控肠道稳态及炎症

10.1038/s41564-019-0659-3

02-03, Article

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Although much research has been done on the diversity of the gut microbiome, little is known about how it influences intestinal homeostasis under normal and pathogenic conditions. Epigenetic mechanisms have recently been suggested to operate at the interface between the microbiota and the intestinal epithelium. We performed whole-genome bisulfite sequencing on conventionally raised and germ-free mice, and discovered that exposure to commensal microbiota induced localized DNA methylation changes at regulatory elements, which are TET2/3-dependent. This culminated in the activation of a set of ‘early sentinel’ response genes to maintain intestinal homeostasis. Furthermore, we demonstrated that exposure to the microbiota in dextran sodium sulfate-induced acute inflammation results in profound DNA methylation and chromatin accessibility changes at regulatory elements, leading to alterations in gene expression programs enriched in colitis- and colon-cancer-associated functions. Finally, by employing genetic interventions, we show that microbiota-induced epigenetic programming is necessary for proper intestinal homeostasis in vivo.

First Authors:
Ihab Ansari

Correspondence Authors:
Yehudit Bergman

All Authors:
Ihab Ansari,Günter Raddatz,Julian Gutekunst,Meshi Ridnik,Daphne Cohen,Monther Abu-Remaileh,Timur Tuganbaev,Hagit Shapiro,Eli Pikarsky,Eran Elinav,Frank Lyko,Yehudit Bergman

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