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DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
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DDX54 regulates transcriptome dynamics during DNA damage response.

Miha Milek1, Koshi Imami1, Neelanjan Mukherjee1

  • 1Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin Institute for Medical Systems Biology, 13125 Berlin, Germany.

Genome Research
|June 10, 2017
PubMed
Summary
This summary is machine-generated.

This study reveals that RNA-binding proteins (RBPs) play a crucial role in the DNA damage response (DDR). Specifically, the RNA helicase DDX54 enhances the splicing of pre-mRNAs, promoting cell survival after genotoxic stress.

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Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Genetics

Background:

  • The DNA damage response (DDR) is critical for maintaining genomic stability.
  • Post-transcriptional gene regulation's role in the DDR is not well understood.
  • RNA-binding proteins (RBPs) are key regulators of gene expression.

Purpose of the Study:

  • To identify RBPs that interact with polyadenylated transcripts upon genotoxic stress.
  • To investigate the function of the RNA helicase DDX54 in the DDR.
  • To understand how DDX54 influences pre-mRNA splicing during DNA damage.

Main Methods:

  • Systematic identification of RBPs binding to poly(A)+ RNA in human breast carcinoma cells exposed to ionizing radiation (IR).
  • Functional analysis of DDX54, including its interactions and role in splicing.
  • Assessment of DDX54's impact on cell survival after IR exposure.

Main Results:

  • Over 260 proteins, including nucleolar proteins, increased their binding to poly(A)+ RNA after IR.
  • DDX54 was identified as an immediate-to-early DDR regulator.
  • DDX54 enhances splicing of IR-induced pre-mRNAs with weak acceptor splice sites, reducing intron retention and increasing processing rates.
  • DDX54 promotes cell survival following IR exposure.

Conclusions:

  • RBPs, particularly DDX54, are significant regulators of the DDR.
  • DDX54's function in splicing is essential for efficient DNA damage repair and cell survival.
  • Uncharacterized RBPs may represent novel targets for understanding and treating DDR-related pathologies.