Clerici Michela, PhD

Associate Professor in Genetics
Michela Clerici BtBs UNIMIB

 

room 5051, building U3, tel. +39 02 6448 3547

lab 5055, building U3, tel. +39 02 6448 3557

michela.clerici@unimib.it

Research Group

Ronzani Fabio – Master student
lab 5055/5051, building U3, tel.+39 02 6448 3557/3547, f.ronzani1@campus.unimib.it

Keywords
DNA damage, Genome stability, DNA replication, Telomeres, ATM

The activity is focused on the following research lines
Health research area BtBs UNIMIB
Health

Cancer

Research interest

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.

Research areas

mechanisms maintaining genome stability: DNA damage cehckpoint, control of DNA replication in stress conditions, repair of DNA double-strand breaks.

Research projects

Selected publications

- 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.

International and national collaborations


Clerici’s Lab – #ClericiLab_BtBs
last update September 2020