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ATM-related Tel1 associates with double-strand breaks through an Xrs2-dependent mechanism

Daisuke Nakada1, Kunihiro Matsumoto, Katsunori Sugimoto

  • 1Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-0814, Japan.

Genes & Development
|August 19, 2003
PubMed

Insights

Tel1 protein associates with DNA double-strand breaks (DSBs) via the Xrs2 protein's C terminus. This association is crucial for activating DNA damage responses, including cell survival and Rad53 phosphorylation.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Budding yeast TEL1 encodes a protein kinase homologous to ATM.
  • Xrs2 is an Nbs1 homolog that forms a complex with Mre11 and Rad50.
  • These proteins are involved in DNA double-strand break (DSB) repair and DNA damage response pathways.

Purpose of the Study:

  • To investigate the mechanism of Tel1 association with DSBs.
  • To determine the role of the Xrs2 C terminus in Tel1 recruitment and DNA damage response.
  • To elucidate the functional relationship between Tel1, Xrs2, and DNA damage signaling.

Main Methods:

  • Yeast genetics and molecular biology techniques.
  • Analysis of protein association with DSBs using Tel1 and Xrs2 mutants.
  • Assessment of DNA degradation, cell survival, and Rad53 phosphorylation after DNA damage induction.

Main Results:

  • Tel1 associates with DSBs through a mechanism dependent on the Xrs2 C terminus.
  • Xrs2 is required for DNA degradation at DSBs, but its C-terminal truncation does not impair this process.
  • Both Tel1 and the Xrs2 C terminus are essential for cell survival and Rad53 phosphorylation following DNA damage.

Conclusions:

  • Tel1 recruitment to DNA lesions, mediated by the Xrs2 C terminus, is a critical step for activating DNA damage responses.
  • The C terminus of Xrs2 plays a distinct role in Tel1 association and DNA damage signaling compared to its role in DNA degradation.

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