The cooperative action of CSB, CSA, and UVSSA target TFIIH to DNA damage-stalled RNA polymerase II

Yana van der Weegen, Hadar Golan-Berman, Tycho E. T. Mevissen, Katja Apelt, Román González-Prieto, Joachim Goedhart, Elisheva E. Heilbrun, Alfred C. O. Vertegaal, Diana van den Heuvel, Johannes C. Walter, Sheera Adar and Martijn S. Luijsterburg ()
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Yana van der Weegen: Leiden University Medical Center
Hadar Golan-Berman: The Hebrew University of Jerusalem
Tycho E. T. Mevissen: Harvard Medical School
Katja Apelt: Leiden University Medical Center
Román González-Prieto: Leiden University Medical Center
Joachim Goedhart: University of Amsterdam
Elisheva E. Heilbrun: The Hebrew University of Jerusalem
Alfred C. O. Vertegaal: Leiden University Medical Center
Diana van den Heuvel: Leiden University Medical Center
Johannes C. Walter: Harvard Medical School
Sheera Adar: The Hebrew University of Jerusalem
Martijn S. Luijsterburg: Leiden University Medical Center

Nature Communications, 2020, vol. 11, issue 1, 1-16

Abstract: Abstract The response to DNA damage-stalled RNA polymerase II (RNAPIIo) involves the assembly of the transcription-coupled repair (TCR) complex on actively transcribed strands. The function of the TCR proteins CSB, CSA and UVSSA and the manner in which the core DNA repair complex, including transcription factor IIH (TFIIH), is recruited are largely unknown. Here, we define the assembly mechanism of the TCR complex in human isogenic knockout cells. We show that TCR is initiated by RNAPIIo-bound CSB, which recruits CSA through a newly identified CSA-interaction motif (CIM). Once recruited, CSA facilitates the association of UVSSA with stalled RNAPIIo. Importantly, we find that UVSSA is the key factor that recruits the TFIIH complex in a manner that is stimulated by CSB and CSA. Together these findings identify a sequential and highly cooperative assembly mechanism of TCR proteins and reveal the mechanism for TFIIH recruitment to DNA damage-stalled RNAPIIo to initiate repair.

Date: 2020
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DOI: 10.1038/s41467-020-15903-8

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