Gabriella Viero
e-mail: viero AT science.unitn.it
affiliation: Università di Trento
research area(s): Cancer Biology
Course:
Biomolecular Sciences
University/Istitution: Università di Trento
University/Istitution: Università di Trento
Current affiliation:
Post-doc fellowship at the Laboratory of Translational Genomics under the supervision of Prof. Alessandro Quattrone, Center for Integrative Biology (CiBio), University of Trento. Research topic: “Ribonucleoparticles complexes: molecular mechanism and their implications”.
Educational and Academic background:
Bachelor in Biological Sciences, University of Padua, 7 July 1999.
Ph.D. in Biotechnologies applied to Biomedical Sciences, University of Verona, 8 June 2006.
Research experience:
November 1999- February 2002 Fellowship at the Centro di Fisica degli Stati Aggregati CNR-ITC di Povo (Tn) Italy
January 2002-Dicembre2005 PhD fellowship, University of Verona and Institute of Biophysics, CNR (Trento) Italy
February- April 2006 PhD fellowship ITC-CNR Institute of Biophysics (Trento) Italy
August 2006-February 2008 Post-doc fellowship at the Departement of Physics, University of Trento, and CNR Institute of Biophysics CNR Italy
Since March 2008 Post-doc fellowship at the Laboratory of Translational Genomics – Center for Integrative Biology, University of Trento Italy
Teaching experience:
2008/2009 Teaching support for the Cellular Biology Course, Bachelor Degree in Sciences and Biomolecular Technologies, University of Trento (Italy).
2009/2010 Teaching support for the Cellular Biology Course, Bachelor Degree in Sciences and Biomolecular Technologies, University of Trento (Italy).
2010/2011 Teaching Biology Course, Master Degree in Informatics, University of Trento (Italy).
Post-doc fellowship at the Laboratory of Translational Genomics under the supervision of Prof. Alessandro Quattrone, Center for Integrative Biology (CiBio), University of Trento. Research topic: “Ribonucleoparticles complexes: molecular mechanism and their implications”.
Educational and Academic background:
Bachelor in Biological Sciences, University of Padua, 7 July 1999.
Ph.D. in Biotechnologies applied to Biomedical Sciences, University of Verona, 8 June 2006.
Research experience:
November 1999- February 2002 Fellowship at the Centro di Fisica degli Stati Aggregati CNR-ITC di Povo (Tn) Italy
January 2002-Dicembre2005 PhD fellowship, University of Verona and Institute of Biophysics, CNR (Trento) Italy
February- April 2006 PhD fellowship ITC-CNR Institute of Biophysics (Trento) Italy
August 2006-February 2008 Post-doc fellowship at the Departement of Physics, University of Trento, and CNR Institute of Biophysics CNR Italy
Since March 2008 Post-doc fellowship at the Laboratory of Translational Genomics – Center for Integrative Biology, University of Trento Italy
Teaching experience:
2008/2009 Teaching support for the Cellular Biology Course, Bachelor Degree in Sciences and Biomolecular Technologies, University of Trento (Italy).
2009/2010 Teaching support for the Cellular Biology Course, Bachelor Degree in Sciences and Biomolecular Technologies, University of Trento (Italy).
2010/2011 Teaching Biology Course, Master Degree in Informatics, University of Trento (Italy).
Our work ranges from computational, systems-level representations of translation-centred networks to their mechanistic dissection in mammalian cells, and to the causative role of their derangement in cancer and neurodegeneration. Specific projects are:
* Computational reconstruction of sequence-dependent translational control networks in whole genomes. Structural and sequence features clustered in the 5’ and 3’ UTRs of mRNAs dictate their fate in the cytoplasm, by the recruitment of RNA binding proteins and non-coding RNAs. By an in silico approach involving annotation of 5’ and 3’ untranslated regions of mRNAs from literature data and motif discovery algorithms we want to look at genes as specific combinations of signals for the mRNA metabolism, which can allow predictions on the shape of post-transcriptional networks. These predictions will be confirmed by benchmarking experiments in cultured cell models.
* The translational network of the “poly(A)-derived superfamily” of RNA binding proteins. Using bioinformatics-based phylogenetic recontruction we are tracing the evolutive history of a group of paralogous genes conserved between invertebrates and vertebrates, and most likely derived by the ancestral poly(A)-binding protein. This group, including the PABP, ELAV, BRUNO and TIA protein families, represents the major cluster of orthologs among RRM-bearing RNA binding proteins in genomes, and is characterized by a variety of regulated and overlapping functions among which sequence-dependent translational control. By a combination of computational and systems-based approaches including RIP-chip and microarray-based polysomal profiling, we are starting to define the function of this macromolecular networking machine in dictating the translational status of the array of bound mRNAs.
* Sequence-dependent translational control derangement in cancer onset and progression. Recent findings point out to the deregulation of translational control by altered signalling pathways as a leading cause of cancer onset and progression. We are conducting a systematic analysis of the involvement of some RNA binding proteins and ribosomal proteins, the major final targets of these pathways, in solid tumors.
* Activity imbalance of ELAV proteins in high risk neuroblastoma. Neuroblastoma is a neural crest-derived tumor which represents the major cause of death in infants. A particularly aggressive form of this cancer is cytogenetically characterized by two recurrent lesions, monoallelic loss of region in the p arm of chromosome 1 and amplification of the MYCN oncogene. Both these alterations can be causally related to alterations in the activity of members of the ELAV family of RNA binding proteins, physiologically involved in the transition from neural stem cells to differentiating neurons. We hypothesize that ELAV protein alteration of activity is a determinant of neuroblastoma progression, and a possible therapeutic target.
* Translational control of synaptic plasticity in memory and memory-impairing disorders by the ELAV network. Previous studies by the group leader involved for the first time post-transcriptional control of gene expression in cognition, demonstrating activation of ELAV proteins as a necessary process for spatial memory encoding. Preliminary data are now demostrating lesions in the ELAV network as a possible determinant of late-onset Alzheimer disease, by affecting the non-amylodogenic pathway in neurons.
* Computational reconstruction of sequence-dependent translational control networks in whole genomes. Structural and sequence features clustered in the 5’ and 3’ UTRs of mRNAs dictate their fate in the cytoplasm, by the recruitment of RNA binding proteins and non-coding RNAs. By an in silico approach involving annotation of 5’ and 3’ untranslated regions of mRNAs from literature data and motif discovery algorithms we want to look at genes as specific combinations of signals for the mRNA metabolism, which can allow predictions on the shape of post-transcriptional networks. These predictions will be confirmed by benchmarking experiments in cultured cell models.
* The translational network of the “poly(A)-derived superfamily” of RNA binding proteins. Using bioinformatics-based phylogenetic recontruction we are tracing the evolutive history of a group of paralogous genes conserved between invertebrates and vertebrates, and most likely derived by the ancestral poly(A)-binding protein. This group, including the PABP, ELAV, BRUNO and TIA protein families, represents the major cluster of orthologs among RRM-bearing RNA binding proteins in genomes, and is characterized by a variety of regulated and overlapping functions among which sequence-dependent translational control. By a combination of computational and systems-based approaches including RIP-chip and microarray-based polysomal profiling, we are starting to define the function of this macromolecular networking machine in dictating the translational status of the array of bound mRNAs.
* Sequence-dependent translational control derangement in cancer onset and progression. Recent findings point out to the deregulation of translational control by altered signalling pathways as a leading cause of cancer onset and progression. We are conducting a systematic analysis of the involvement of some RNA binding proteins and ribosomal proteins, the major final targets of these pathways, in solid tumors.
* Activity imbalance of ELAV proteins in high risk neuroblastoma. Neuroblastoma is a neural crest-derived tumor which represents the major cause of death in infants. A particularly aggressive form of this cancer is cytogenetically characterized by two recurrent lesions, monoallelic loss of region in the p arm of chromosome 1 and amplification of the MYCN oncogene. Both these alterations can be causally related to alterations in the activity of members of the ELAV family of RNA binding proteins, physiologically involved in the transition from neural stem cells to differentiating neurons. We hypothesize that ELAV protein alteration of activity is a determinant of neuroblastoma progression, and a possible therapeutic target.
* Translational control of synaptic plasticity in memory and memory-impairing disorders by the ELAV network. Previous studies by the group leader involved for the first time post-transcriptional control of gene expression in cognition, demonstrating activation of ELAV proteins as a necessary process for spatial memory encoding. Preliminary data are now demostrating lesions in the ELAV network as a possible determinant of late-onset Alzheimer disease, by affecting the non-amylodogenic pathway in neurons.
M. Dalla Serra, M. Coraiola, G. Viero, M. Comai, C. Potrich, M.Ferreras, L. Baba-Moussa, D.A. Colin; G .Menestrina, S. Bhakdi and G. Prevost. Staphylococcus aureus bicomponent gamma-hemolysins, HlgA, HlgB and HlgC can form mixed pores containing all components. J. Chem. Inf. Mod. 2005 45:1539-45.
G. Viero, R. Cunaccia, G. Prevost, S. Werner, H. Monteil, D. Keller, O. Joubert, G. Menestrina and M. Dalla Serra. Homologous versus heterologous interactions in the bicomponent staphylococcal γ-hemolysins pore Biochem. J. 2006 394: 217-25.
Joubert O, G. Viero, D. Keller, E. Martinez, DA. Colin, H. Monteil, L. Mourey, M. Dalla Serra, G. Prevost. Engineered covalent leucotoxin heterodimers form functional pores: insights into S-F interactions. Biochem J. 2006 396(2):381-9.
K. Kristan, G. Viero, P. Macek, M. Dalla Serra and G. Anderluh. The equinatoxin Nterminus is transferred across planar lipid membranes and help sto stabilize the transmembrane pore. FEBS J. 2007 274 (2):539-50.
G. Viero, A. Gropuzzo, O. Joubert, D. Keller, G. Prevost, M. Dalla Serra A molecular pin to study the dynamics of beta-barrel formation in pore-forming toxins on erythrocytes: a sliding model. Cell Mol Life Sci. 2008 Jan;65(2):312-23.
S.*Rabzelj, G.*Viero, G. Anderluh, M. Dalla Serra and E. Žerovnik. Interaction with model membranes and pore formation by human stefin B variants; studying the native and prefibrillar states. FEBS J. 2008 May;275(10):2455-66 * co-first author
K. Kristan, G. Viero, M. Dalla Serra, P. Macek, G. Anderluh. Molecular mechanism of pore formation by actinoporins. Toxicon. 2009 Dec 15;54(8):1125-34.
T. Praper, A. Sonnen, G. Viero, A. Kladnik, CJ Froelich, G. Anderluh, M. Dalla Serra, R. Gilbert Human perforin employs different avenues to damage membranes. J Biol Chem. 2010 Oct 2
G. Viero, R. Cunaccia, G. Prevost, S. Werner, H. Monteil, D. Keller, O. Joubert, G. Menestrina and M. Dalla Serra. Homologous versus heterologous interactions in the bicomponent staphylococcal γ-hemolysins pore Biochem. J. 2006 394: 217-25.
Joubert O, G. Viero, D. Keller, E. Martinez, DA. Colin, H. Monteil, L. Mourey, M. Dalla Serra, G. Prevost. Engineered covalent leucotoxin heterodimers form functional pores: insights into S-F interactions. Biochem J. 2006 396(2):381-9.
K. Kristan, G. Viero, P. Macek, M. Dalla Serra and G. Anderluh. The equinatoxin Nterminus is transferred across planar lipid membranes and help sto stabilize the transmembrane pore. FEBS J. 2007 274 (2):539-50.
G. Viero, A. Gropuzzo, O. Joubert, D. Keller, G. Prevost, M. Dalla Serra A molecular pin to study the dynamics of beta-barrel formation in pore-forming toxins on erythrocytes: a sliding model. Cell Mol Life Sci. 2008 Jan;65(2):312-23.
S.*Rabzelj, G.*Viero, G. Anderluh, M. Dalla Serra and E. Žerovnik. Interaction with model membranes and pore formation by human stefin B variants; studying the native and prefibrillar states. FEBS J. 2008 May;275(10):2455-66 * co-first author
K. Kristan, G. Viero, M. Dalla Serra, P. Macek, G. Anderluh. Molecular mechanism of pore formation by actinoporins. Toxicon. 2009 Dec 15;54(8):1125-34.
T. Praper, A. Sonnen, G. Viero, A. Kladnik, CJ Froelich, G. Anderluh, M. Dalla Serra, R. Gilbert Human perforin employs different avenues to damage membranes. J Biol Chem. 2010 Oct 2
No projects are available to students for the current accademic year.