SUMO2 conjugation of PCNA facilitates chromatin remodeling to resolve transcription-replication conflicts

Min Li, Xiaohua Xu, Chou-Wei Chang, Li Zheng, Binghui Shen and Yilun Liu ()
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Min Li: Beckman Research Institute, City of Hope
Xiaohua Xu: Beckman Research Institute, City of Hope
Chou-Wei Chang: Beckman Research Institute, City of Hope
Li Zheng: Beckman Research Institute, City of Hope
Binghui Shen: Beckman Research Institute, City of Hope
Yilun Liu: Beckman Research Institute, City of Hope

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: Abstract During DNA synthesis, DNA replication and transcription machinery can collide, and the replication fork may temporarily dislodge RNA polymerase II (RNAPII) to resolve the transcription-replication conflict (TRC), a major source of endogenous DNA double-strand breaks (DSBs) and common fragile site (CFS) instability. However, the mechanism of TRC resolution remains unclear. Here, we show that conjugation of SUMO2, but not SUMO1 or SUMO3, to the essential replication factor PCNA is induced on transcribed chromatin by the RNAPII-bound helicase RECQ5. Proteomic analysis reveals that SUMO2-PCNA enriches histone chaperones CAF1 and FACT in the replication complex via interactions with their SUMO-interacting motifs. SUMO2-PCNA enhances CAF1-dependent histone deposition, which correlates with increased histone H3.1 at CFSs and repressive histone marks in the chromatin to reduce chromatin accessibility. Hence, SUMO2-PCNA dislodges RNAPII at CFSs, and overexpressing either SUMO2-PCNA or CAF1 reduces the incidence of DSBs in TRC-prone RECQ5-deficient cells.

Date: 2018
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DOI: 10.1038/s41467-018-05236-y

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