一种独特的淋巴细胞增强剂结合因子1 (LEF1) 的异型在表观遗传上限制了EBV的重新激活,以维持病毒延迟
B J H Ward1,2,3, Kanchanjunga Prasai1, Danielle L Schaal1,2,3
1Department of Microbiology and Immunology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana, United States of America.
PLoS pathogens
|December 19, 2023
概括
淋巴细胞增强剂结合因子1 (LEF1) 通过抑制病毒重新激活来维持爱斯坦-巴尔病毒 (EBV) 延迟. 这涉及表观遗传变化和关键病毒基因的染色质重塑,影响癌症的发展.
科学领域:
- 病毒学 病毒学
- 分子生物学分子生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 在瘤学瘤学.
背景情况:
- 爱斯坦-巴尔病毒 (EBV) 在相关癌症中建立了潜在的感染,遗传和表观遗传变化阻碍了细胞分化和病毒重新激活.
- 之前的研究表明,EBV上皮感染后淋巴细胞增强剂结合因子1 (LEF1) 水平增加,感染后持续存在,并在鼻癌和伯基特淋巴瘤中观察到.
研究的目的:
- 研究LEF1在爱斯坦-巴尔病毒 (EBV) 生命周期中的作用.
- 为了确定LEF1是否直接与EBV基因组结合并调节病毒基因表达.
主要方法:
- 在EBV基因组的分析中,以确定Wnt-响应元素.
- CUT&RUN测序用于映射潜伏EBV基因组中的LEF1结合位.
- 通过siRNA介导的特定LEF1异型的消耗和病毒基因表达的评估.
- 分析LEF1结合位点的组织素乙化变化.
主要成果:
- 在EBV基因组中发现了20多个Wnt反应元素,这表明直接结合LEF1.
- LEF1与EBV基因组区域结合,包括BZLF1和BSLF1基因.
- 一种截断的LEF1异型 (ΔN LEF1) 在转录上抑制了Lytic基因并对抗EBV的重新激活.
- LEF1的枯竭导致EBV结合部位的基因素乙化增加,这表明它在染色质重塑中的作用.
结论:
- 在维持EBV延迟方面,LEF1发挥着新的作用.
- LEF1通过压制性染色质重塑关键的溶液循环因子来限制EBV的活性.
- 这种 ΔN LEF1 异型是 EBV 流性基因表达的关键抑制剂.
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