Irene ChioloGabilan Assistant Professor of Biological Sciences
Phone: (213) 821-3163
Office: RRI 203
Chiolo Lab Website
- Ph.D. Genetics, University of Milan, 2005
- Postdoctoral Fellow, Lawrence Berkeley National Lab / UC Berkeley, 2007-2011
- Postdoctoral Fellow, Institute of Molecular Oncology Foundation, Milan, 2006-2007
- Assistant Professor of Biological Sciences, University of Southern California, 01/2013-
- Lawrence Berkeley National Lab, Guest Faculty
- USC/Norris Cancer Center, Full Member, http://uscnorriscancer.usc.edu/about/programs/
- Chiolo, I., Tang, J., Georgescu, W., Costes, S. V. (2013). Nuclear dynamics of radiation-induced foci in euchromatin and heterochromatin. Mutation Research.
- Chiolo, I., Minoda, A., Colmenares, S. U., Polyzos, A., Costes, S. V., Karpen, G. H. (2011). Double-strand breaks in heterochromatin move outside of a dynamic HP1a domain to complete recombinational repair. Cell. Vol. 144 (5), pp. 732-44.
- Chiolo*, I., Robert*, T., Vanoli*, F., Shubassi, G., Bernstein, K. A., Rothstein, R., Botrugno, O. A., Parazzoli, D., Oldani, A., Minucci, S., Foiani, M. (2011). HDACs link the DNA damage response, processing of double-strand breaks and autophagy. Nature. Vol. 471 (7336), pp. 74-9. *Co-first authors.
- Costes, S. V., Chiolo, I., Pluth, J. M., Barcellos-Hoff, M. H., Jakob, B. (2010). Spatiotemporal characterization of ionizing radiation induced DNA damage foci and their relation to chromatin organization. Mutation Research. Vol. 704 (1-3), pp. 78-87.
- Tavecchio, M., Simone, M., Erba, E., Chiolo, I., Liberi, G., Foiani, M., D'Incalci, M., Damia, G. (2008). Role of homologous recombination in trabectedin-induced DNA damage. Eur J Cancer. Vol. 44 (4), pp. 609-18.
- Chiolo, I., Saponaro, M., Baryshnikova, A., Kim, J., Seo, Y., Liberi, G. (2007). The human F-Box DNA helicase FBH1 faces Saccharomyces cerevisiae Srs2 and postreplication repair pathway roles. Mol Cell Biol. Vol. 27 (21), pp. 7439-50.
- Chiolo, I., Carotenuto, W., Maffioletti, G., Petrini, J. H., Foiani, M., Liberi, G. (2005). Srs2 and Sgs1 DNA helicases associate with Mre11 in different subcomplexes following checkpoint activation and CDK1-mediated Srs2 phosphorylation. Mol Cell Biol. Vol. 25 (13), pp. 5738-51.
- Liberi, G., Maffioletti, G., Lucca, C., Chiolo, I., Baryshnikova, A., Cotta-Ramusino, C., Lopes, M., Pellicioli, A., Haber, J. E., Foiani, M. (2005). Rad51-dependent DNA structures accumulate at damaged replication forks in sgs1 mutants defective in the yeast ortholog of BLM RecQ helicase. Genes Dev. Vol. 19 (3), pp. 339-50.
- Liberi, G., Chiolo, I., Pellicioli, A., Lopes, M., Plevani, P., Muzi-Falconi, M., Foiani, M. (2000). Srs2 DNA helicase is involved in checkpoint response and its regulation requires a functional Mec1-dependent pathway and Cdk1 activity. EMBO J. Vol. 19 (18), pp. 5027-38.
- USC Endowed Professorship, Gabilan Assistant Professor of Biological Sciences, 1/1/2013-
- American Society for Cell Biology (ASCB), 2007-
- The Genetics Society of America (GSA), 2007-
Academic Appointment, Affiliation, and Employment History
Description of Research
Summary Statement of Research Interests
Research in Professor Chiolo’s laboratory focuses on the mechanisms of DNA repair in heterochromatin. This nuclear domain is highly enriched in repetitive sequences and prone to generating chromosome rearrangements during double-strand break (DSB) repair, but repair processes are still mostly unknown. Our studies have revealed surprising dynamics triggered by DSBs in heterochromatin: the entire domain expands and repair sites display a dramatic relocalization to the euchromatic space, while repair progression is tightly regulated in space and time. This pathway is essential for accurate repair in heterochromatin, because its deregulation results in aberrant recombination and genome instability. Which molecular mechanisms control heterochromatin dynamics and how they influence repair are still unclear. Using the Drosophila system, currently the best working model for heterochromatin repair studies, research in my lab aims to identify the mechanisms involved, and to address how they protect genome integrity at cellular and organismal levels. This research will ultimately contribute to our understanding of human diseases associated with genome instability, including developmental defects and cancer.
Double-strand break repair in heterochromatin, epigenetics, homologous recombination, genome stability, Smc5/6 complex, Drosophila model system
Affiliations with Research Centers, Labs, and Other Institutions
Honors and Awards
Service to the Profession
- Department of Biological Sciences
- University of Southern California
- Allan Hancock Foundation Building
- Los Angeles, CA 90089-0371
- Phone: (213) 740 - 1109
- Email: firstname.lastname@example.org