The findings of this research, carried out by Sandra Muñoz Galván, María Luisa García Rubio, Pedro Ortega, José Francisco Ruiz, Sonia Jimeno, Benjamín Pardo, Belén Gómez González and Andrés Aguilera, have been brought together in the article A new role for Rrm3 in repair of replication-born DNA breakage by sister chromatid recombination published by the review PLoS Genet in its May 2017 edition.
The replication of DNA is one of the cellular processes during which DNA is most vulnerable. During this stage, the replication forks can meet obstacles that cause their blockage or even the appearance of breaks in the DNA. The breaks in DNA that occur during replication require a specific mechanism for their repair, the recombination mechanism. In this project, it was shown that Rrm3, a protein that travels beside the replication forks, has a role in this process of repair by recombination, so avoiding genetic instability.
Understanding the physiological mechanisms that cause or, as in this case, prevent genetic instability is a basic question in Molecular Biology and Biomedicine which is of vital importance in the research against cancer, given that genetic instability is a distinctive feature of tumorous cells. In fact, genetic instability appears to be associated with cancer from its first stages of development and can be involved both as a cause of cancer (tumorigenesis) and in the generation of genetic variation within a tumour itself (intratumoral heterogeneity).