Giordano Liberi
Giordano Liberi
affiliation: Istituto di Genetica Molecolare CNR Pavia
research area(s): Molecular Biology, Genetics And Genomics
Course: Genetics, Molecular and Cellular Biology
University/Istitution: Università di Pavia

Born in Cassano D"Adda (Milan) Italy, on 11th July 1968. Italian citizenship.

Institute of Molecular Genetics, National Research Council of Italy (IGM-CNR)
Via Abbiategrasso 207, 27100, Pavia, Italy.
Ph. +39 0382-546364
web link:

1996: Degree of specialization at "School of Applied Genetics", University of Milan.
1993: Degree in Biological Sciences at the University of Milan.

September 2011-present: Researcher at Institute of Molecular Genetics, National Research Council (IGM-CNR) of Pavia.
2001-2011: Unit Head and Staff Scientist in the Prof. M.Foiani"s group at the IFOM Institute Foundation of Milan.
1998-2001: Permanent member of research staff at the University of Milan.
1996-1998: Telethon Foundation Post-Doctoral Fellow at the University of Milan.

We are interested in understanding the molecular mechanisms that promote genome instability, which is a hallmark of cancer and many neurodegenerative diseases. Our work has been focused on a group of evolutionarily conserved DNA/RNA helicases in Saccharomyces cerevisiae with a role in preserving replication fork integrity.

Since 1998, in the field of Biological Sciences, lab supervisor of undergraduate and PhD students at the University of Milan and Pavia, as well as PhD students at European School of Molecular Medicine at IFOM.

G.Liberi is author/co-author of 28 papers on peer-reviewed international journals and 2 book chapters. Total Impact Factor: 341.4; H index: 16 (ISI Web of knowledge).

- "Giovanni Magni" prize assigned by "Adriano Buzzati-Traverso" Foundation for original contribution to the scientific research on the field of genetic microorganisms from 1999 to 2000. Article rewarded: Liberi et al., 2000. EMBO J 19: 5027-5038.
- AIRC Grant "Characterization of DNA helicases involved in the DNA damage response using yeast as a model system", 2001-2002.
- AIRC Grant "Functional characterization of DNA repair helicases protecting genome integrity", 2006-2008.
- Telethon Grant "Molecular characterization of SEN1/SETX"controlled pathways defective in the AOA2 and ASL4 neurodegenerative syndromes", 2009-2011.
- AIRC Grant "Functional analysis of UvrD and RecQ helicases-mediated DNA repair network", 2009-2011.
We are interested in understanding the mechanisms that generate genome instability, which is a hallmark of cancer and many neurodegenerative disorders. Genome instability is induced by double and single strand breaks that can trigger non-conservative recombinational repair events. Our research has been focused on a group of conserved DNA/RNA helicase in Saccharomyces cerevisiae whose human counterparts are inactivated in certain neurodegenerative diseases or cancer-prone syndromes. These DNA/RNA helicases have been involved in preventing unwanted recombinational repair events during S-phase when replication fork arrests because of DNA damage or collides with transcription, which is a natural impediment for replication. The aim of our research is to characterize how these DNA/RNA helicases contribute to maintain replication fork integrity using genetic, genomic and molecular biology approaches, as it is easy applicable in the yeast model system.
1. Liberi G, and Foiani M. (2010). The double life of Holliday junctions. Cell Res 20: 611-613.
2. Carotenuto W, and Liberi G. (2010). Mitotic inter-homolog junctions accumulate at damaged DNA replication forks in recQ mutants. DNA repair 9: 661-669.
3. Saponaro M, Callahan D, Zheng X, Krejci L, Haber JE, Klein HL, and Liberi G. (2010). Cdk1 targets Srs2 to complete synthesis-dependent strand annealing and to promote recombinational repair. PLoS Genet 6: e1000858.
4. Kerrest A, Anand RP, Sundararajan R, Bermejo R, Liberi G, Dujon B, Freudenreich CH, and Richard G-F. (2009). SRS2 and SGS1 prevent chromosomal breaks and stabilize triplet repeats by restraining recombination. Nat Struct Mol Biol 16: 159-167.
5. Tavecchio M, Simone M, Erba E, Chiolo I, Liberi G, Foiani M, D'Incalci M, and Damia G. (2008). Role of homologous recombination in trabectedin-induced DNA damage. Eur J Cancer 44: 609-611.
6. Cogliati M, Esposto MC, Liberi G, Tortorano AM, and Viviani MA. (2007). Cryptococcus neoformans typing by PCR fingerprinting using (GACA)4 primer: a new ligth on the basis of Cryptococcus neoformans genome project data. J Clin Microbiol 45: 3427-3430.
7. Theis JF, Dershowitz A, Irene C, Maciariello C, Tobin ML, Liberi G, Tabrizifard S, Korus M, Fabiani L, and Newlon CS. (2007). Identification of Mutations That Decrease The Stability of a Fragment of S. cerevisiae Chromosome III Lacking Efficient Replicators. Genetics 177:1445-1458.
8. Chiolo I, Saponaro M, Baryshnikova A, Kim JH, Seo YS, and Liberi G. (2007). The human F-box DNA helicase FBH1 faces S. cerevisiae Srs2 and post-replication repair pathway roles. Mol Cell Biol (cover) 27: 7439-7450.
9. Branzei D, Sollier J, Liberi G, Zhao X, Maeda D, Enomoto T, Seki M, Ohta K, and Foiani M. (2006). Ubc9- and Mms21- mediated sumoylation counteracts recombinogenic events at damaged replication forks. Cell 127: 509-522.
10. Liberi G, Cotta-Ramusino C, Lopes M, Sogo J, Conti C, Bensimon A, and Foiani M. (2006). Methods to study replication fork collapse in budding yeast. Methods Enzymol 409: 442-462.
11. Chiolo I, Carotenuto W, Maffioletti G, Petrini JHJ, Foiani M, and Liberi G. (2005). Srs2 and Sgs1 DNA helicases associate with Mre11 in different sub-complexes following checkpoint activation and CDK1-mediated Srs2 phosphorylation. Mol Cell Biol 25: 5738-5751.
12. Liberi G, Maffioletti G, Lucca C, Chiolo I, Baryshnikova A, Cotta-Ramusino C, Lopes M, Pellicioli A, Haber JE, and 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 19: 339-350.
No projects are available to students for the current accademic year.