Cip29 is phosphorylated following activation of the DNA damage response in Xenopus egg extracts

Janet Holden1, Elaine M Taylor1, Howard D Lindsay1

  • 1Lancaster Medical School, Faculty of Health and Medicine, Lancaster University, Lancaster, United Kingdom.

Plos One
|July 18, 2017
PubMed

Insights

The DNA damage response modifies the RNA export factor Cip29 via ATM kinase. This damage-dependent phosphorylation suggests Cip29 may regulate gene expression following DNA damage.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Genetics

Background:

  • DNA damage triggers complex cellular responses, including repair and altered gene expression.
  • RNA processing factors are emerging as key players in DNA damage signaling and gene regulation.
  • The role of RNA export factors in DNA damage response pathways is not well understood.

Purpose of the Study:

  • To investigate the DNA damage-dependent modification of the putative RNA export factor Cip29.
  • To determine the signaling pathways and specific sites involved in Cip29 modification.
  • To assess the role of Cip29 in DNA repair processes.

Main Methods:

  • Utilized a Xenopus laevis egg extract system to study DNA damage responses.
  • Analyzed DNA double-strand break-induced phosphorylation of Cip29.
  • Investigated the involvement of ATM kinase in Cip29 modification.
  • Identified the specific phosphorylation site on Cip29.
  • Assessed Cip29's role in DNA end-joining.

Main Results:

  • Cip29 undergoes rapid phosphorylation in response to DNA double-strand breaks.
  • This modification is dependent on ATM kinase activity.
  • A conserved serine residue was identified as the damage-dependent phosphorylation site.
  • Cip29 was found not to be essential for efficient DNA end-joining in egg extracts.

Conclusions:

  • Cip29 is a novel target of the DNA damage response pathway.
  • The phosphorylation of Cip29 is regulated by ATM kinase.
  • The damage-dependent modification of Cip29 likely relates to its role in gene expression regulation after DNA damage.
  • Cip29 is not directly involved in DNA end-joining repair.

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