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Lack of effect of RuvB-like proteins on DNA damage signaling activation

Anastas Gospodinov1, Boyka Anachkova

  • 1Institute of Molecular Biology, Bulgarian Academy of Sciences, Acad G. Bonchev Str. 21, Sofia 1113, Bulgaria. agg@bio21.bas.bg

Zeitschrift Fur Naturforschung. C, Journal of Biosciences
|April 2, 2010
PubMed

Insights

The TIP60 chromatin modification complex, including TIP48 and TIP49, is not required for the activation of ATM kinase in DNA damage response. Our findings indicate this complex does not function upstream of ATM in DNA damage signaling.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Ataxia telangiectasia mutated (ATM) kinase is crucial for DNA damage response.
  • ATM activation involves phosphorylation of histone H2AX, recruiting repair proteins.
  • The TIP60 complex, including TIP48 and TIP49, was recently implicated in ATM acetylation and activation.

Purpose of the Study:

  • To investigate the role of TIP48 and TIP49 in ATM activation and DNA damage signaling.
  • To determine if the TIP60 complex is essential for ATM-mediated H2AX phosphorylation and cell cycle arrest.

Main Methods:

  • Depletion of TIP48 and TIP49 using silencing techniques.
  • Irradiation of depleted cells to induce DNA double-strand breaks.
  • Monitoring of cell cycle distribution and H2AX phosphorylation as indicators of ATM activation.

Main Results:

  • Depletion of TIP48 and TIP49 did not affect cell cycle distribution after irradiation.
  • H2AX phosphorylation levels remained unchanged in TIP48- and TIP49-silenced cells.
  • These results suggest TIP48 and TIP49 are not required for ATM activation.

Conclusions:

  • The TIP60 chromatin modification complex, comprising TIP48 and TIP49, is not essential for ATM activation.
  • The TIP60 complex does not appear to function upstream of ATM in the DNA damage response pathway.
  • This study refutes the proposed role of the TIP60 complex in ATM activation signaling.

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