IGM-CNR Director

Dr. Giuseppe Biamonti

Via Abbiategrasso, 207

27100 PAVIA

tel. +39 0382 546322

fax. +39 0382 546381

e-mail: direttoreigm.cnr.it

PEC: direttore.igmpec.cnr.it


Curriculum Vitae




My research activity focuses on two fundamental aspects of human cell biology: DNA replication and RNA metabolism. 

DNA replication is the process of producing two identical replicas from one original DNA molecule. Replication of the large human genome follows a tightly controlled spatio-temporal program, which is only partially understood. I contributed to the isolation and detailed molecular characterization of the DNA replication origin associated with the human lamin B2 gene, which is now a reference model for studies in this field. I also validated the replicon model in human cells by showing that a very short DNA sequence centered on the lamin B2 origin is able to support initiation of DNA replication when integrated into ectopic position of the genome. DNA replication occurs in “replication factories” whose number and distribution changes during the S-phase. The nature of these nuclear entities is still largely unexplored. I reported the identification of the first protein motif able to mediate the recruitment of replicative enzymes to replication factories. 

It is increasingly evident that RNA plays crucial roles in a number of cellular functions, from gene expression regulation to chromatin organization. 

My research interest in this field is centered on two main aspects. I have identified one of the first members of the growing family of long non-coding RNAs. This molecule is produced in human cells after heat shock through transcription of large pericentromeric heterochromatic portions of the genome formed by long tandem arrays of Satellite III repetitive DNA. Heat shock induces a drastic change in the epigenetic organization of these regions that become euchromatic and transcribed. Long non-coding Satellite III RNA remain associated with transcription sites and recruit a specific subset of splicing factors giving rise to novel nuclear structures called nuclear stress bodies. In this way SatIII RNAs affect the nuclear organization and perturb alternative splicing regulation of gene expression. 

Alternative splicing is a potent mechanisms of gene expression regulation that expands the coding capacity of the genome leading to the production of different mRNA molecules from a single primary gene transcript. I am interested in the role of alternative splicing in cancer progression. In particular, the involvement of alternative splicing in the epithelial to mesenchymal transition (EMT), a complex cell reorganization event physiologically important during embryogenesis but also exploited by cancer cells for the metastatic spreading of tumors. I have shown that splicing regulator SRSF1 can induce EMT by modulating the splicing profile of the Ron proto-oncogene. SRSF1 promotes the production of a Ron isoform that confers an invasive phenotype to the cells. Interestingly, the level of SRSF1 is controlled through an alternative splicing event that induces the degradation of SRSF1 transcripts via the non-sense mediated RNA decay pathway. This regulatory mechanism is controlled by the signal transduction pathway identified by Erk. These studies indicate that splicing factors may control cell identity acting as effectors of signal transduction pathways.



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