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Interplays between ATM/Tel1 and ATR/Mec1 in sensing and signaling DNA double-strand breaks

Elisa Gobbini1, Daniele Cesena, Alessandro Galbiati

  • 1Dipartimento di Biotecnologie e Bioscienze, Università di Milano-Bicocca, Piazza della Scienza 2, 20126 Milan, Italy.

DNA Repair
|August 20, 2013
PubMed

Insights

DNA double-strand breaks (DSBs) pose significant risks to genome integrity. This review details how DNA-end structures activate key protein kinases, ATM/Tel1 and ATR/Mec1, to manage the DNA damage response.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • DNA double-strand breaks (DSBs) are critical DNA lesions that threaten genome integrity.
  • Cellular responses, including DNA damage checkpoints, are essential for maintaining genomic stability.
  • Master regulators like ATM/ATR (mammals) and Tel1/Mec1 (yeast) orchestrate these responses.

Purpose of the Study:

  • To review the initial stages of DNA double-strand break (DSB) processing.
  • To elucidate the role of DNA-end structures in activating ATM/Tel1 and ATR/Mec1 signaling pathways.
  • To explain the coordinated and reciprocal activation of these key kinases.

Main Methods:

  • Literature review of early DSB processing mechanisms.
  • Analysis of signal transduction pathways involved in DNA damage response.
  • Examination of the interplay between DNA-end structures and kinase activation.

Main Results:

  • DSB processing involves specific DNA-end structures that act as crucial signaling platforms.
  • These structures facilitate the orderly and reciprocal activation of ATM/Tel1 and ATR/Mec1 kinases.
  • This coordinated activation is vital for effective DNA repair and cell cycle control.

Conclusions:

  • The structure of DNA ends is a key determinant in initiating the DNA damage response.
  • ATM/Tel1 and ATR/Mec1 kinases are activated in a regulated manner to ensure genome stability.
  • Understanding these early events is fundamental to comprehending DNA repair and checkpoint control.
Keywords:
ATM/Tel1ATR/Mec1CheckpointDNA double-strand breaksMRN/MRXResection

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