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首页> 外文期刊>Molecular and Cellular Biology >Poly(ADP-Ribose) Polymerase 1 and Ste20-Like Kinase hKFC Act as Transcriptional Repressors for Gamma-2 Herpesvirus Lytic Replication
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Poly(ADP-Ribose) Polymerase 1 and Ste20-Like Kinase hKFC Act as Transcriptional Repressors for Gamma-2 Herpesvirus Lytic Replication

机译：聚（ADP-核糖）聚合酶1和Ste20样激酶hKFC充当转录抑制因子，用于γ-2疱疹病毒裂解复制。

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The replication and transcription activator (RTA) of gamma-2 herpesvirus is sufficient to drive the entire virus lytic cycle. Hence, the control of RTA activity should play an important role in the maintenance of viral latency. Here, we demonstrate that cellular poly(ADP-ribose) polymerase 1 (PARP-1) and Ste20-like kinase hKFC interact with the serine/threonine-rich region of gamma-2 herpesvirus RTA and that these interactions efficiently transfer poly(ADP-ribose) and phosphate units to RTA. Consequently, these modifications strongly repressed RTA-mediated transcriptional activation by inhibiting its recruitment onto the promoters of virus lytic genes. Conversely, the genetic ablation of PARP-1 and hKFC interaction or the knockout of the PARP-1 gene and activity considerably enhanced gamma-2 herpesvirus lytic replication. Thus, this is the first demonstration that cellular PARP-1 and hKFC act as molecular sensors to regulate RTA activity and thereby, herpesvirus latency.
机译：γ-2疱疹病毒的复制和转录激活因子（RTA）足以驱动整个病毒裂解周期。因此，RTA活性的控制应在维持病毒潜伏期中发挥重要作用。在这里，我们证明了细胞多聚（ADP-核糖）聚合酶1（PARP-1）和Ste20样激酶hKFC与伽玛2疱疹病毒RTA富含丝氨酸/苏氨酸的区域相互作用，并且这些相互作用有效地转移了poly（ADP-核糖）和磷酸酯单位的RTA。因此，这些修饰通过抑制RTA募集到病毒裂解基因的启动子上来强烈抑制RTA介导的转录激活。相反，PARP-1和hKFC相互作用的遗传消融或PARP-1基因和活性的敲除大大增强了γ-2疱疹病毒的裂解复制。因此，这是细胞PARP-1和hKFC充当分子传感器来调节RTA活性，从而调节疱疹病毒潜伏期的第一个证明。

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