Asghar Asim, Vladimirova Olga, Sobotka Asher, Hayden James, Wickramasinghe Jayamanna, Dheekollu Jayaraju, Minakuchi Moeko, Yoon Leena, Murphy Maureen E, Nishikura Kazuko, Lieberman Paul M
The Wistar Institute, Philadelphia, Pennsylvania, United States of America.
PLoS Pathog. 2025 Aug 18;21(8):e1013029. doi: 10.1371/journal.ppat.1013029. eCollection 2025 Aug.
Transcription-replication conflicts frequently occur at repetitive DNA elements involved in genome maintenance functions. The KSHV terminal repeats (TR) function as the viral episome maintenance element when bound by the viral encoded nuclear antigen LANA. Here, we show that transcription-replication conflicts occur at or near LANA binding sites in the TR. We show by proximity ligation assay (PLA) that PCNA and RNAPII colocalize with LANA-nuclear bodies (LANA-NBs). Using DNA-RNA-IP (DRIP) assays with S9.6 antibody, we demonstrate that R-loops form at the TR. We find that these R-loops are also associated with histone H3pS10 a marker for R-loops associated with transcription-replication conflicts. Inhibitors of RNAPII eliminated R-loop formation at TR and reduced active histone modifications H3K4me3 and H3K27ac, with a corresponding increase in heterochromatic H3K9me3. RNAPII inhibitors also disrupted LANA binding to the TR, but did not eliminate LANA-NBs. We show that LANA can induce R-loops on a plasmid containing 8, but not 2 copies of the TR, and that the N-terminal histone binding function of LANA is required for this activity. RNaseH treatment eliminated R-loops and reduced LANA binding to the TR. Taken together, our study indicates that LANA induces histone modifications associated with RNA and DNA polymerase activity and the formation of R-loops that correlate with episome maintenance function. These findings provide new insights into mechanisms of KSHV episome maintenance during latency and more generally for genome maintenance of repetitive DNA.
转录-复制冲突经常发生在参与基因组维持功能的重复DNA元件处。当被病毒编码的核抗原LANA结合时,卡波西肉瘤相关疱疹病毒(KSHV)末端重复序列(TR)作为病毒附加体维持元件发挥作用。在此,我们表明转录-复制冲突发生在TR中LANA结合位点处或其附近。我们通过邻近连接分析(PLA)表明,增殖细胞核抗原(PCNA)和RNA聚合酶II(RNAPII)与LANA核体(LANA-NBs)共定位。使用S9.6抗体进行DNA-RNA免疫沉淀(DRIP)分析,我们证明在TR处形成R环。我们发现这些R环也与组蛋白H3pS10相关,H3pS10是与转录-复制冲突相关的R环的标志物。RNAPII抑制剂消除了TR处的R环形成,并减少了活性组蛋白修饰H3K4me3和H3K27ac,同时异染色质H3K9me3相应增加。RNAPII抑制剂还破坏了LANA与TR的结合,但并未消除LANA-NBs。我们表明,LANA可以在含有8个而非2个TR拷贝的质粒上诱导R环形成,并且LANA的N端组蛋白结合功能是该活性所必需的。核糖核酸酶H处理消除了R环,并减少了LANA与TR的结合。综上所述,我们的研究表明,LANA诱导与RNA和DNA聚合酶活性相关的组蛋白修饰以及与附加体维持功能相关的R环形成。这些发现为KSHV潜伏期附加体维持机制以及更普遍的重复DNA基因组维持机制提供了新的见解。