期刊
NATURE STRUCTURAL & MOLECULAR BIOLOGY
卷 19, 期 3, 页码 276-U29出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nsmb.2224
关键词
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资金
- Fondation pour la Recherche Medicale en France [SPF20091217677]
- Human Frontiers Science program (HFSP CDA)
- Agence Nationale de la Recherche (ANR)
- Centre National de la Recherche Scientifique (CNRS, ATIP)
- Institut National du Cancer (INCA)
- European FP7 framework (Marie Curie Reintegration)
- NIH [CA50519]
- Cancer Research Institute of Texas [RP110465]
DNA double-strand break (DSB) repair interferes with ongoing cellular processes, including replication and transcription. Although the process of replication stalling upon collision of replication forks with damaged DNA has been extensively studied, the fate of elongating RNA polymerase II (RNAPII) that encounters a DSB is not well understood. We show that the occurrence of a single DSB at a human RNAPII-transcribed gene leads to inhibition of transcription elongation and reinitiation. Upon inhibition of DNA protein kinase (DNAPK), RNAPII bypasses the break and continues transcription elongation, suggesting that it is not the break per se that inhibits the processivity of RNAPII, but the activity of DNAPK. We also show that the mechanism of DNAPK-mediated transcription inhibition involves the proteasome-dependent pathway. The results point to the pivotal role of DNAPK activity in the eviction of RNAPII from DNA upon encountering a DNA lesion.
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