Beatrice joined Sophie Polo‘s team in September 2017 as a postdoctoral fellow. During her PhD at San Raffaele Scientific Institute in Milan, Italy, she identified a new role for the histone demethylase JARID1C in the maintenance of genome stability through heterochromatin condensation after DNA replication. She also characterized that JARID1C has a role in DNA replication origin firing. She then moved to the Dana Farber Cancer Institute in Boston, MA, where, under the supervision of Alan D’Andrea, she characterized a new mechanism of chemoresistance in BRCA2-deficient tumors that is mediated by the downregulation of EZH2 activity at stalled replication forks, which in turn abolishes the activity of the endonuclease MUS81. In Sophie Polo‘s lab, Beatrice is studying the role of histone H3.3 oncogenic mutations in inducing genomic instability in human tumors, with the support of a Marie Curie reintegration grant. She obtained a permanent staff scientist position (CNRS) in 2018.

PUBLICATIONS

• Ferrand J.*, Rondinelli B.*, Polo S.E. Histone variants: guardians of genome integrity. Cells, 9:2424, 2020. *: equal contribution
• Rondinelli B., Gogola E., Yücel H., Duarte A.A., van de Ven M., van der Sluijs R., Konstantinopoulos P.A., Jonkers J., Ceccaldi R., Rottenberg S., D‘Andrea A.D. EZH2 promotes degradation of stalled replication forks by recruiting MUS81 through histone H3 trimethylation. Nat Cell Biol, 19:1371-1378, 2017.
• Kais Z.*, Rondinelli B.*, Holmes A., O‘Leary C., Kozono D., D‘Andrea A.D.§ and Ceccaldi R§. FANCD2 maintains fork stability in BRCA1/2-deficient tumors allowing for alternative end-joining DNA repair. Cell Rep, 15: 2488-99, 2016. * co-first authors; § co-corresponding authors
• Ceccaldi R., Rondinelli B., D‘Andrea A.D. Repair Pathway Choices and Consequences at the Double-Strand Break. Trends Cell Biol, 26: 52-64 , 2016.
• Rondinelli B., Rosano D., Antonini E., Frenquelli M., Montanini L., Huang D., Segalla S., Yoshihara K., Amin S.B., Lazarevic D., Verhaak R.G., Futreal P.A., Di Croce L., Chin L., Cittaro D., Tonon G. Histone demethylase JARID1C inactivation triggers genomic instability in sporadic renal cancer. J Clin Invest, 1125: 4625-37, 2015.
• Rondinelli B., Schwerer H., Antonini E., Gaviraghi M., Lupi A., Frenquelli M., Cittaro D., Segalla S., Lemaitre J.M., Tonon G. H3K4me3 demethylation by the histone demethylase KDM5C/JARID1C promotes DNA replication origin firing. Nucleic Acids Res, 43: 2560-74 , 2015.