Functions and regulation of the MRX complex at DNA double-strand breaks
Authors:Elisa Gobbini1, Corinne Cassani1, Matteo Villa1, Diego Bonetti2 and Maria Pia Longhese1
doi: 10.15698/mic2016.08.517
Volume 3, pp. 329 to 337, published 27/07/2016.
1 Dipartimento di Biotecnologie e Bioscienze, Università di Milano-Bicocca, Piazza della Scienza 2, 20126 Milan, Italy.
2 Institute of Molecular Biology gGmbH (IMB), 55128 Mainz, Germany.
Keywords:
double-strand break, resection, MRX, nucleases, Tel1, Rif2, Sae2.
Corresponding Author(s):
Conflict of interest statement:
The authors declare that they have no conflict of interest.
Please cite this article as:
Elisa Gobbini, Corinne Cassani, Matteo Villa, Diego Bonetti and Maria Pia Longhese (2016). Functions and regulation of the MRX complex at DNA double-strand breaks. Microbial Cell 3(8): 329-337. doi: 10.15698/mic2016.08.517
© 2016 Gobbini et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
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.