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Updated: Aug 24, 2026

Application of Laser Micro-irradiation for Examination of Single and Double Strand Break Repair in Mammalian Cells
Published on: September 5, 2017
Functions and regulation of the MRX complex at DNA double-strand breaks
Elisa Gobbini1, Corinne Cassani1, Matteo Villa1
1Dipartimento di Biotecnologie e Bioscienze, Università di Milano-Bicocca, Piazza della Scienza 2, 20126 Milan, Italy.
Abstract:
DNA double-strand breaks (DSBs) pose a serious threat to genome stability and cell survival. Cells possess mechanisms that recognize DSBs and promote their repair through either homologous recombination (HR) or non-homologous end joining (NHEJ). The evolutionarily conserved Mre11-Rad50-Xrs2 (MRX) complex plays a central role in the cellular response to DSBs, as it is implicated in controlling end resection and in maintaining the DSB ends tethered to each other. Furthermore, it is responsible for DSB signaling by activating the checkpoint kinase Tel1 that, in turn, supports MRX function in a positive feedback loop. The present review focuses mainly on recent works in the budding yeast Saccharomyces cerevisiae to highlight structure and regulation of MRX as well as its interplays with Tel1.
Insights
The Mre11-Rad50-Xrs2 (MRX) complex is crucial for DNA double-strand break (DSB) repair and genome stability. This review highlights MRX structure, regulation, and its interplay with Tel1 in Saccharomyces cerevisiae.
Area of Science:
- Molecular Biology
- Genetics
- Cellular Biology
Background:
- DNA double-strand breaks (DSBs) threaten genome stability and cell survival.
- Cells repair DSBs via homologous recombination (HR) or non-homologous end joining (NHEJ).
- The Mre11-Rad50-Xrs2 (MRX) complex is vital for DSB recognition, repair, and signaling.
Purpose of the Study:
- To review recent findings on the structure and regulation of the MRX complex.
- To elucidate the interplay between the MRX complex and Tel1 kinase.
- To focus on studies in the budding yeast Saccharomyces cerevisiae.
Main Methods:
- Literature review of recent research.
- Analysis of structural and regulatory mechanisms of MRX.
- Examination of MRX-Tel1 interactions.
Main Results:
- MRX controls DSB end resection and tethers broken DNA ends.
- MRX initiates DSB signaling by activating Tel1.
- Tel1 supports MRX function through a positive feedback loop.
Conclusions:
- The MRX complex is a key regulator of DNA double-strand break repair pathways.
- MRX and Tel1 form a critical regulatory network for maintaining genome stability.
- Understanding MRX and Tel1 interactions provides insights into DNA repair mechanisms.
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