About
General interests and key questions
We study how genomes have evolved, only looking at DNA sequence regularities and genomic rules. DNA contains a code that is similar to human languages, and is an ensembl of laws with several degrees of freedom. Chomsky "the father of linguistics" and Shannon "the father of information theory" are two historical figures sharing similar points of view. They both believed that a code should be regulated by rules in order to restrict the amount of choices that are allowed to be transmitted by its source. The transmitter possesses also a certain amount of degrees of freedom that is, in my opininion, tha hard drive of evolution. However, evolution can be also explained by thermodynamics and, especially, through the concept of entropy that is the synonym of disorder or tendendcy to equilibrium in its "Boltzmannian" interpretation. Starting from the pubblication of the book "What is life?" written by the Nobel prize Erwin Schrodinger in 1944, the origin of life and evolution are now seen not only at level of molecular biology but also as opened physical system adsorbing more energy than the objects in the surroundings.
We recently solved a genome mystery called Chargaff's second parity rule that states that on the two single DNA strands, A=T and C=G. This has been a mistery for over 50 years. Our results suggest that the tendency of Universe to maximum entropy together with the double helix constraints are the driving force of Chargaff's second parity rule and DNA tridimensional structure. Selective biological processes act, instead, as soft drivers, which only under extraordinary circumstances overtake the overall entropy content of the genome. Our mathematical model predicts perfectly the number of reverse complement in real genomes for every kmer length therefore validating our theory (Fariselli&Taccioli et al. 2020, Briefings in Bioinformatics).
We recently contributed to the field of Transposable elements insertions comparing Transposable Elements (TEs) activity among 29 Mammalian families. We recently showed that taxa with high rates of speciation are associated with “hot” genomes (high number of species), whereas taxa with low ones are associated with “cold” genomes (low number of species). These results suggest a remarkable correlation between TE activity and speciation, also being consistent with patterns describing variable rates of differentiation and accounting for the different time frames of the speciation bursts (reviewed in Ricci et. al 2018, Journal of Molecular Evolution).
Regulation of genes by miR-31. MiR-31 is a microRNA deregulated in Esophageal Squamous Cell Carcinoma. In collaboration with Thomas Jefferson University we created a Zinc Deficient rat model that develops a pre-cancer environment in ESCC cells. Our bioinformatic analyses show the miR-31, that is upregulated in pre-cancer rats, regulates chronical inflammation and proliferation pathways through S100A8/9, NFKB, and RAGE. At epigenomic level miR-31 also regulated TFs related to histone modifications in ZD vs Zinc suffient (ZS) normal rats.
Comparative genomics. We are also interested in cancer free animal models. To this aim, we are developing new tools and algorithms in order to identify new markers that lead to cancer resistance.
Population genomics. In collaboration with the colleagues at University of Padova and Bologna we are also studying population genomics in Europeans both using human publicly available datasets and regional data.
Our approach to these goals entails both genomic and evolutionary investigations and combines an interdisciplinary set of expertise, ranging from molecular biology, physics and theory of information.