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耶尔森菌重塑人类巨噬细胞中的表观遗传组蛋白修饰。

Yersinia remodels epigenetic histone modifications in human macrophages.

机构信息

Institute of Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.

Heinrich-Pette-Institute (HPI), Leibniz Institute for Experimental Virology, Research Group Virus Genomics, Hamburg, Germany.

出版信息

PLoS Pathog. 2021 Nov 18;17(11):e1010074. doi: 10.1371/journal.ppat.1010074. eCollection 2021 Nov.

DOI:10.1371/journal.ppat.1010074
PMID:34793580
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8639070/
Abstract

Various pathogens systematically reprogram gene expression in macrophages, but the underlying mechanisms are largely unknown. We investigated whether the enteropathogen Yersinia enterocolitica alters chromatin states to reprogram gene expression in primary human macrophages. Genome-wide chromatin immunoprecipitation (ChIP) seq analyses showed that pathogen-associated molecular patterns (PAMPs) induced up- or down-regulation of histone modifications (HMod) at approximately 14500 loci in promoters and enhancers. Effectors of Y. enterocolitica reorganized about half of these dynamic HMod, with the effector YopP being responsible for about half of these modulatory activities. The reorganized HMod were associated with genes involved in immune response and metabolism. Remarkably, the altered HMod also associated with 61% of all 534 known Rho GTPase pathway genes, revealing a new level in Rho GTPase regulation and a new aspect of bacterial pathogenicity. Changes in HMod were associated to varying degrees with corresponding gene expression, e. g. depending on chromatin localization and cooperation of the HMod. In summary, infection with Y. enterocolitica remodels HMod in human macrophages to modulate key gene expression programs of the innate immune response.

摘要

各种病原体系统地重新编程巨噬细胞中的基因表达，但潜在的机制在很大程度上尚不清楚。我们研究了肠道病原体小肠结肠炎耶尔森氏菌是否会改变染色质状态，以重新编程原代人巨噬细胞中的基因表达。全基因组染色质免疫沉淀（ChIP）seq 分析表明，病原体相关分子模式（PAMPs）在启动子和增强子中约 14500 个基因座诱导了组蛋白修饰（HMod）的上调或下调。耶尔森氏菌的效应物重新组织了大约一半的这些动态 HMod，其中效应物 YopP 负责大约一半的这些调节活性。重新组织的 HMod 与参与免疫反应和代谢的基因有关。值得注意的是，改变的 HMod 也与所有 534 个已知 Rho GTPase 途径基因中的 61%相关，揭示了 Rho GTPase 调节的新水平和细菌致病性的新方面。HMod 的变化与相应基因表达的程度不同，例如取决于染色质定位和 HMod 的合作。总之，小肠结肠炎耶尔森氏菌的感染重塑了人巨噬细胞中的 HMod，以调节先天免疫反应的关键基因表达程序。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/52fe0a867cb3/ppat.1010074.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/8936704cb9a2/ppat.1010074.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/c56ee29ff910/ppat.1010074.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/04810dd92b58/ppat.1010074.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/06b6a1087d12/ppat.1010074.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/8255e471d935/ppat.1010074.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/52fe0a867cb3/ppat.1010074.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/8936704cb9a2/ppat.1010074.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/c56ee29ff910/ppat.1010074.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/04810dd92b58/ppat.1010074.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/06b6a1087d12/ppat.1010074.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/8255e471d935/ppat.1010074.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e6/8639070/52fe0a867cb3/ppat.1010074.g006.jpg

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