M. Clerici research activity has been exploring the mechanisms preserving genome stability in eukaryotes, mainly focusing on the relationships between DNA damage checkpoint, DNA repair and DNA replication, by using the budding yeast Saccharomyces cerevisiae as model system. In particular, her more recent research activity has provided significant insights into the functions of the evolutionarily conserved ATM/Tel1 checkpoint kinase in the repair of DNA double-strand breaks, the response to topoisomerase inhibition, and the signalling of dysfunctional telomeres.
- Menin L, Colombo CV, Maestrini G, Longhese MP, Clerici M. 2019. Tel1/ATM Signaling to the Checkpoint Contributes to Replicative Senescence in the Absence of Telomerase. Genetics 213:411-429. doi: 10.1534/genetics.119.302391.
- Colombo CV, Menin L, Ranieri R, Bonetti D, Clerici M, Longhese MP. 2019 Uncoupling Sae2 Functions in Downregulation of Tel1 and Rad53 Signaling Activities. Genetics 211:515-530. doi: 10.1534/genetics.118.301830.
- Menin L, Ursich S, Trovesi C, Zellweger R, Lopes M, Longhese MP, Clerici M. 2018. Tel1/ATM prevents degradation of replication forks that reverse after topoisomerase poisoning. EMBO Rep. 19 pii: e45535. doi: 10.15252/embr.201745535.
- Colombo CV, Trovesi C, Menin L, Longhese MP, Clerici M. 2017. The RNA binding protein Npl3 promotes resection of DNA double-strand breaks by regulating the levels of Exo1. Nucleic Acids Res. 45:6530-6545. doi: 10.1093/nar/gkx347.