I'm the Director of the Center of Functional Genomics of University of Verona and I'm the Scientific Director of Personal Genomics, a Spin-Off of University of Verona founded in 2011. During the last few years, my lab participated to the sequencing of the Vitis vinifera and Bifidobacterium dentium
genomes, and performed an impressive number of genome wide microarray
analyses of gene expression. The recent development of high density
microarrays prompted us to implement technologies for comparative
genome hybridization, chromatin immunoprecipitation ("ChIP on chip")
and sequence capture for targeted resequencing with 2nd generation
sequencing technologies (deep sequencing). As deep sequencing has
rapidly gained popularity for transcriptome analysis because of its
ability to generate digital and quantitative information and to
discover previously unknown genes, in 2008 we embraced gene expression
analysis based on deep sequencing of the transcriptome (RNA-Seq). Since
then, my lab has continued implementing and developing new wet-lab
methodologies and bioinformatic pipelines for expression data analysis
on genomic scales.
As the sequencing costs dropped, we started sequencing whole human
genomes and exomes, an we became involved in a number of targeted
resequencing projects based on oligo capture and amplicon sequencing.
Whereas the lab is now deeply involved in genomic and transcriptomic
projects with a special focus on the characterization of the "private"
genome that we believe strongly contributes to make the difference
among living organisms belonging to the same specie, I'm now
particulary interested in human genome interpretation
Major equipments for whole genome and transcriptome
sequencing include an Illumina Hiseq 1000 and a Life Technology
Ion Torrent One Touch platform. The lab also uses PacBio data and has also access to three other
sequencers: Illumina GAIIX, Ion Torrent, 454 Roche . The main computing power is given by a Dell R900 (4 Intel Xeon® 7450
6-core and 128 Gb RAM), a Cluster HP DL380 G7 (6 Intel Xeon®
5645 6-core and 144 Gb RAM) and a DELL R911 (2 Intel Xeon 7500 8-core and 512 Gb RAM).
Nitric oxide (NO) is a
highly reactive molecule that rapidly diffuses and permeates cell
membranes. In animals, NO is implicated in a number of diverse
physiological processes such as neurotransmission, vascular smooth
muscle relaxation, and platelet inhibition. It may have beneficial
effects, for example as a messenger in immune responses, but is also
potentially toxic when the antioxidant system is weak and an excess of
reactive oxygen intermediates (ROI) accumuates.
During the last few years NO has been detected also in several plant
species, and the
increasing number of reports on its function in plants have implicated
NO as an important effector of growth, development, and
defense. The broad chemistry of NO involves an array of interrelated
redox forms
with different chemical reactivities, and numerous potential targets of
NO action exist in plants. NO signaling functions depend on its
reactivity and ROI are key modulators of NO in triggering cell death,
although through mechanisms different from those commonly observed in
animals
My laboratory specialises in
the
characterization of
NO functions at cellular and molecular levels in plants. In
collaboration with Chris
Lamb we
made pioneering work towards the discovery of NO function during the
plant hypersensitive disease resistance response. We found that during
the hypersensitive response plant cells accumulate NO, which
co-operates with reactive oxygen species in the induction of
hypersensitive cell death, and functions independently of such
intermediates in the induction of defence related genes (Delledonne et
al., 1998). We then demonstrated that the rates of production and
dismutation of O2- generated during the
oxidative burst play
a crucial role in the modulation and integration of NO/H2O2
signalling in the hypersensitive response (Delledonne et al., 2001).
Due to the many possible mechanisms of NO action, a clear
picture of its involvement in plant resistance to pathogens is far from
being achieved. Our goal is now to characterize and modulate the signal
transduction pathways leading to the hypersensitive disease resistance
response. We are going in deep in the analysis of genes involved in the
hypersensitive cell death and in the establishment of disease
resistance whose expression is under control of NO. We built a NO
fumigation platform that allow us to screen for mutants plants impaired
in the activation of NO-triggered cell death, and we are now
characterizing the first arabidopsis mutants that we have identified.
We
are also focusing on the mechanisms regulating NO level in plant, and
on the identification and characterization of signalling mechanisms
that operate downstream of NO accumulation. In particular, we are
analysing the occurrence of NO-dependent posttranslational
modifications of proteins (S-nitrosylation and Tyr-nitration) to
clarify their biological function and to understand their functional
consequences in physiological and pathophysiological conditions.