The hardwired transcriptional response to DNA damage

Elisheva E. Heilbrun, May Merav, Avital Parnas, Sheera Adar*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

3 Scopus citations

Abstract

There is a complex network of interactions between bulky DNA damages and transcription. Bulky damages block RNA polymerases but also elicit a regulated transcriptional response. At the same time, active transcription enhances the ability to recognize and repair damages. Eventually, transcription is completely shut down until after damages are removed. Recent projects untangle this web of interaction in mammalian cells by applying time-sensitive and high-resolution measurements of damage, repair, and transcription at genome-wide scales. The emerging model indicates the transcriptional response to damage is primarily hardwired in the damaged genomic DNA, and transcription shutdown can be explained almost completely by (1) aborted transcription by blocked RNA polymerases and (2) ubiquitination and degradation of RNA polymerase II after encountering a damage.

Original languageAmerican English
Pages (from-to)1-7
Number of pages7
JournalCurrent Opinion in Systems Biology
Volume19
DOIs
StatePublished - Feb 2020

Bibliographical note

Funding Information:
The authors thank Hadar Golan-Berman for helpful comments. This work was funded by the Israel Science Foundation grants ( 1710/17 ) administered by the Israeli Academy for Science and humanities, the Israel Cancer Association grant ( 20191630 ). SA is the recipient of the Jacob and Lena Joels memorial fund senior lectureship. EEH is the recipient of the Malvina and Solomon Pollack Scholarship fund and the Israel Council for Higher Education scholarship. Figures were generated using BioRender.com .

Funding Information:
The authors thank Hadar Golan-Berman for helpful comments. This work was funded by the Israel Science Foundation grants (1710/17) administered by the Israeli Academy for Science and humanities, the Israel Cancer Association grant (20191630). SA is the recipient of the Jacob and Lena Joels memorial fund senior lectureship. EEH is the recipient of the Malvina and Solomon Pollack Scholarship fund and the Israel Council for Higher Education scholarship. Figures were generated using BioRender.com.

Publisher Copyright:
© 2020 Elsevier Ltd

Keywords

  • DNA damage
  • DNA repair
  • Genomics
  • Nucleotide excision repair
  • RNA polymerase II
  • Transcription
  • UV
  • Ubiquitination

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