Polo Sophie E
Epigenetics & Cell Fate Centre, UMR7216 CNRS, Sorbonne Paris Cité, Paris Diderot University, Paris, France.
EMBO Rep. 2017 May;18(5):659-660. doi: 10.15252/embr.201744052. Epub 2017 Mar 23.
Transcription is tightly regulated in response to DNA damage. Rapid and transient pausing of RNA polymerase II (RNAPII) is indeed critical to restrict the production of aberrant transcripts from damaged loci and to prevent deleterious collisions between transcription and repair machineries. Yet, how DNA lesions signal to the transcription machinery to coordinate DNA repair with transcriptional silencing is not fully elucidated. In this issue of , Awwad 1 bring a new piece to the puzzle by identifying the negative transcription elongation factor NELF as a critical player in this process. They demonstrate that NELF is recruited to DNA double‐strand breaks (DSBs) near transcriptionally active genes in a poly(ADP‐ribose)‐ and RNAPII‐dependent manner to promote transcriptional repression and facilitate DSB repair.
转录过程受到严格调控以应对DNA损伤。RNA聚合酶II（RNAPII）的快速短暂暂停对于限制受损基因座异常转录本的产生以及防止转录与修复机制之间的有害碰撞至关重要。然而，DNA损伤如何向转录机制发出信号以协调DNA修复与转录沉默尚未完全阐明。在本期杂志中，Awwad等人通过鉴定负转录延伸因子NELF作为这一过程中的关键参与者，为这一谜题增添了新的内容。他们证明，NELF以聚（ADP-核糖）和RNAPII依赖的方式被招募到转录活跃基因附近的DNA双链断裂（DSB）处，以促进转录抑制并促进DSB修复。
