Centro Andaluz de Biología Molecular y Medicina Regenerativa
Sonia Jimeno González

e-mail: sonia.jimeno@cabimer.es

Main Research lines

  • DNA repair and DNA damage response: We are characterizing the role G-quadruplexes and RNA modifications in the DNA resection process
  • RNA editing and cancer: We are trying to stablish a possible role of RNA editing in the process of tumor adaptation to treatments
  • Aicardi goutiéres syndrome: We are looking for new drugs that might be used in the future as a treatment in this genetically inherited rare disease.

DNA is constantly confronting different DNA damaging sources that endanger its integrity. Thus, cells have perfectioned several DNA repair pathways to preserve genomic integrity. When both DNA strands get simultaneously damaged, there is not an intact template from which restore the DNA sequence and DSBs are generated, this kind of injuries being considered one of the most cytotoxic ones. In order to conserve genomic stability, cells have developed a well-regulated signalling cascade, known as the DNA Damage Response (DDR), to detect and repair these DNA alterations. Given the importance of DNA repair in tumor progression, there are many anti-cancer therapies based on the reduced capability of some tumor cells to cope with an exogenous source of DNA damage due to defective repair 3 as is the case of BRCA1-related tumors. Indeed, all radiotherapies and many targeted and general chemotherapies are effective only because cancer cells are more sensitive to DNA damaging agents. Moreover, some specific therapies against recombination-defective tumors (such as BRCA1 or 2-related malignancies) like PARP inhibitors are currently showing promising results in different clinical trials and the development of resistance to those PARP inhibitors is the main concern about these new treatments.

RNA editing alters RNA sequences by the action of specific deaminases that convert one base into another. Every mammalian transcript can be subjected to RNA editing. RNA editing can be classified into several categories, including adenosine-to-inosine (A-to-I) deamination, which is accomplished by a family of RNA-specific adenosine deaminases known as ADARs. This family is formed by ADAR1, ADAR2 (also known as ADARB1), and ADAR3; however, only ADAR1 and ADAR2 have been shown to present catalytic activity. Moreover, A-to-I editing has been proposed to be involved in the pathogenesis of cancer.

I am interested in the connection of these two so important nuclear processes, we have recently discovered that ADAR1 and ADAR2 are indeed factors with a role in the DDR (Jimeno et. al, 2021). Indeed, we have shown that the general pattern of ADAR2-mediated A-to-I editing changes upon DSB formation, such changes being depend on the DDR. As a consequence, ADAR2 is required for the maintenance of genomic integrity. Strikingly, ADAR2 role in the maintenance of genomic integrity is related with a role in homologous recombination and to its ability to edit DNA:RNA hybrids, such structures increasing when ADAR2 is depleted. Based on our findings, we propose an RNA-editing DNA Damage Response (REDAR) which is essential for DNA repair, contributing to the maintenance of genomic integrity. Specifically, we postulate that upon the triggering of the DDR, REDAR is activated and then, ADAR proteins, are mobilized from its usual targets to new ones, where they could increase the editing of a small fraction of yet-undisclosed mRNAs, whose role in the DDR is still to be clarified.

The Aicardi-Goutières syndrome (AGS) is an inflammatory autoimmune disorder that was first described in 1984 by Jean Aicardi and Françoise Goutières. In general it was characterized by an early onset encephalopathy with a high number of white blood cells in the cerebrospinal fluid (CSF) and basal ganglia calcification. All of these are symptoms typically associated with an immune response to congenital viral infection, however it seemed to be no traces of such infection. Besides these symptoms, it is common in the majority of AGS patients to find elevated levels of type I-Interferon (I-IFN) in CSF. This might be responsible of the inflammatory phenotype observed in children with the disease .At this moment, it is known that the syndrome is a genetically heterogeneous disease that can be caused by mutations in seven different genes, and amongst them we find ADAR1.

Principal Investigator:

TÍTULO: “Regulation of DNA break repair by the circadian clock”
Fecha de comienzo/1/1/2020 Fecha de fin/31/12/2022

TÍTULO: “The RNA editing DNA damage response (REDAR) as a driving force of tumour adaptation”.
Fecha de comienzo/1/12/2022 Fecha de fin/2/12/2024


  1. ADAR-mediated RNA editing of DNA:RNA hybrids is required for DNA double strand break repair Jimeno, S*., Prados-Carvajal, R., Fernández-Ávila, M.J., …Visa, N., Huertas, P*. Nature Communications, 2021, 12(1), 5512. *co-corresponding authors.
  2. The Effect of Atypical Nucleic Acids Structures in DNA Double Strand Break Repair: A Tale of R-loops and G-Quadruplexes Camarillo, R., Jimeno, S*., Huertas, P*. *co-corresponding authors. Frontiers in Genetics, 2021, 12, 742434
  3. The Emerging Role of RNA Modifications in DNA Double-Strand Break Repair Jimeno, S., Balestra, F.R., Huertas, P. Frontiers in Molecular Biosciences, 2021, 8, 664872
  4. Preparation of a radiobiology beam line at the 18 MeV proton cyclotron facility at CNA Baratto-Roldán, A., Jiménez-Ramos, M.D.C., Jimeno, S., …Cortés-Giraldo, M.A., Espino, J.M.Physica Medica, 2020, 74, pp. 19–29
  5. EXOSC10 is required for RPA assembly and controlled DNA end resection at DNA double-strand breaks Domingo-Prim, J., Endara-Coll, M., Bonath, F., …. Jimeno, S……Huertas, P., Visa, N. Nature Communications, 2019, 10(1), 2135
  6. The role of RNA and RNA-related proteins in the regulation of DNA double strand break repair pathway choice Jimeno, S., Prados-Carvajal, R., Huertas, P. DNA Repair, 2019, 81, 102662
  7. Controlling the balance between chromosome break repair pathways Jimeno, S., Mejías-Navarro, F., Prados-Carvajal, R., Huertas, P. Advances in Protein Chemistry and Structural Biology, 2019, 115, pp. 95–134
  8. Jimeno, S*., Camarillo, R., Mejías-Navarro, F., Fernández-Ávila, M.J., Soria-Bretones, I., Prados-Carvajal, R., Huertas, P*. “The Helicase PIF1 Facilitates Resection over Sequences Prone to Forming G4 Structures”. Cell Reports, 24;pp: 1001-1013, Septiembre 2018. *co-corresponding authors.
  9. Rosario Prados-Carvajal, Ana López-Saavedra, Cristina Cepeda-García, Sonia Jimeno and Pablo Huertas.”Multiple roles of the splicing complex SF3B in DNA end resection and homologous recombination” DNA Repair (2018). 10.1016/j.dnarep.2018.04.003.
  10. Jimeno S, Herrera-Moyano E, Ortega P, Aguilera. “Differential effect of the overexpression of Rad2/XPG family endonucleases on genome integrity in yeast and human cells”. DNA Repair. 2017: Sep;57:66-75. doi: 10.1016/j.dnarep.2017.06.030.
  11. Muñoz-Galván S, García-Rubio M, Ortega P, Ruiz JF, Jimeno S, Pardo B, Gómez-González B, Aguilera A.“A new role for Rrm3 in repair of replication-born DNA breakage by sister chromatid recombination.” PLoS Genet. 2017: May 5;13(5):e1006781.
  12. Sonia Jimeno, María Jesús Fernández-Ávila, Cristina Cepeda-García, Andrés Cruz-García, Daniel Gómez-Cabello and Pablo Huertas. “Neddylation inhibits CtIP-mediated resection and regulates DNA double strand break repair pathway choice”. Nucleic Acids Res. 2015: Jan;43(2):987-99. doi: 10.1093/nar/gku1384.
  13. Gomez-Cabello D, Jimeno S, Fernández-Ávila MJ, Huertas P. “New tools to study DNA double-strand break repair pathway choice.” PLoS One. 2013: Oct 14;8(10):e77206.
  14. Muñoz-Galván S*, Jimeno S*, Rothstein R, Aguilera A. “Histone H3K56 acetylation, Rad52, and non-DNA repair factors control double-strand break repair choice with the sister chromatid.” PLoS Genet. 2013: Jan;9(1). *Equal contribution.
  15. Qvist P, Huertas P, Jimeno S, Nyegaard M, Jackson SP, Borglum AD. “CtIP mutations cause Seckel and Jawad syndromes” PLOS Genetics . 2011: October e1002310.
  16. Jimeno S, Tous C, García-Rubio ML, Ranes M, González-Aguilera C, Marín A, Aguilera A. “New suppressors of THO mutations identify Thp3 (Ypr045c)-Csn12 as a protein complex involved in transcription elongation.” Mol Cell Biol. 2011: Feb;31(4):674-85.
  17. Rondón AG, Jimeno S, Aguilera A. “The interface between transcription and mRNP export: from THO to THSC/TREX-2”. Biochim Biophys Acta. 2010: Aug;1799(8):533-8.
  18. Jimeno S and Aguilera A “ The THO complex as a key mRNP biogénesis factor in development and differentiation.”. J Biol. 2010;9(1):6.
  19. Faza MB, Kemmler S, Jimeno S, González-Aguilera C, Aguilera A, Hurt E, Panse VG. “Sem1 is a functional component of the nuclear pore complex-associated messenger RNA export machinery.” J Cell Biol. 2009: Mar 23;184(6):833-46.
  20. García-Rubio M, Chávez S, Huertas P, Tous C, Jimeno S, Luna R, Aguilera A. “Different physiological relevance of yeast THO/TREX subunits in gene expression and genome integrity”. Mol Genet Genomics. 2008: Feb;279(2):123-32.
  21. Sonia Jimeno, Maria García-Rubio, Rosa Luna and A. Aguilera. “A reduction in RNA polymerase II initiation rate suppresses hyper-recombination and transcription elongation impairment of THO mutants” Mol Genet Genomics. 2008: Oct;280(4):327-36.
  22. Grenon M, Costelloe T, Jimeno S, O’shaughnessy A, Fitzgerald J, Zgheib O, Degerth L, Lowndes NF. “Docking onto chromatin via the Saccharomyces cerevisiae Rad9 Tudor domain” Yeast. 2007 Feb;24(2):105-19.
  23. S. Jimeno, R. Luna Garcia-Rubio M and A. Aguilera. “Tho1, a novel hnRNP, and Sub2 provide alternative pathways for mRNP biogenesis in yeast THO mutants.” Mol Cell Biol. 2006 Jun;26(12):4387-98.
  24. Toh GW, O’Shaughnessy AM, Jimeno S, Dobbie IM, Grenon M, Maffini S, O’Rorke A and Lowndes NF. “Histone H2A phosphorylation and H3 methylation are required for a novel Rad9 DSB repair function following checkpoint activation.”DNA Repair. 2006: Jun 10;5(6):693-703
  25. Luna R, Jimeno S, Marín M, Huertas P, García-Rubio M, Aguilera A “Interdependence between transcription and mRNP processing and export, and its impact on genetic stability”. Mol Cell. 2005: Jun 10;18(6):711-22.
  26. A.G. Rondón, S. Jimeno, María García-Rubio and A. Aguilera “Molecular evidece that the THO/TREX complex is required for efficient transcription elongation”. JBC, 278, 40, 39037-39043 (2003).
  27. S. Jimeno, A.G. Rondón, R. Luna and A. Aguilera. “The yeast THO complex and mRNA export factors link RNA metabolism with transcription and genome instability” EMBO J, 21, 3526 -3535 (2002).

Participación en grupos PAIDI financiados:
– Grupo PAIDI “BIO-026-Metabolismo del DNA”

Premios de investigación recibidos:
– Premio del X concurso de Ideas de Negocio en categoría de investigadoras (fase ideas).
– Premio del X concurso de Ideas de Negocio en categoría de personal docente e investigador (fase final).

Tesis doctorales dirigidas:
– Una tesis doctoral dirigida en el año TÍTULO: “Regulación de la reparación de los cortes de doble cadena en el ADN: Papel de la neddilación de proteínas”. DOCTORANDO: María Jesús Fernández Ávila; año 2016.
– Tres tesis doctorales en realización para ser defendidas en el año 2023.