Extensive cooperation of immune master regulators IRF3 and NFκB in RNA Pol II recruitment and pause release in human innate antiviral transcription.
Extensive cooperation of immune master regulators IRF3 and NFκB in RNA Pol II recruitment and pause release in human innate antiviral transcription.
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DOI：
10.1016/j.celrep.2013.07.043
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发表时间：
2013-09-12
期刊：
影响因子：
8.8
通讯作者：
Horvath CM
中科院分区：
文献类型：
--
作者：
Freaney JE;Kim R;Mandhana R;Horvath CM
转录因子 IRF3 和 NFκB 被外部刺激（包括病毒感染）激活，转移到细胞核并结合对免疫和炎症重要的基因组靶标。为了研究人类抗病毒基因调控网络中 RNA 聚合酶 II (Pol II) 的招募和延伸，在病毒感染的初始阶段进行了全面的全基因组分析。结果揭示了 IRF3 和 NFκB 与 Pol II 和相关机制的广泛整合，并暗示了抗病毒转录的新伙伴。分析表明，聚合酶从头招募和暂停聚合酶的刺激释放共同作用来控制病毒诱导的基因激活。除了已知的 mRNA 编码位点外，IRF3 和 NFκB 还可刺激先前与抗病毒转录无关的区域的转录，包括编码新型病毒诱导性 RNA (nviRNA) 的大量未注释位点。这些 nviRNA 在不同细胞类型中广泛由病毒感染诱导，代表了以前被忽视的对病毒感染的细胞反应。
Transcription factors IRF3 and NFκB, are activated by external stimuli, including virus infection, to translocate to the nucleus and bind genomic targets important for immunity and inflammation. To investigate RNA polymerase II (Pol II) recruitment and elongation in the human antiviral gene regulatory network, a comprehensive genome-wide analysis was conducted during the initial phase of virus infection. Results reveal extensive integration of IRF3 and NFκB, with Pol II and associated machinery, and implicate new partners for antiviral transcription. Analysis indicates that both de novo polymerase recruitment and stimulated release of paused polymerase work together to control virus-induced gene activation. In addition to known mRNA-encoding loci, IRF3 and NFκB, stimulate transcription at regions not previously associated with antiviral transcription, including abundant unannotated loci that encode novel virus-inducible RNAs (nviRNAs). These nviRNAs are widely induced by virus infections in diverse cell types and represent a previously overlooked cellular response to virus infection.
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