Daniela Leronni, PhD, has been a research instructor at the University of Pittsburgh Department of Neurological Surgery since January 2017.
She earned her BS/MS in biological sciences with a thesis in molecular biology at the University of Bari, Italy, in 2007. She completed her doctorate in genetics and molecular evolution at the University of Bari, in 2011
Dr. Leronni’s early work as a PhD student and research assistant at the University of Bari from 2008 to 2011 focused on the functional characterization of genetics elements in the genome of model organisms with a low number of chromosomes, such as Drosophila Melanogaster (fruit fly) and Culex Quinquefasciatus (southern house mosquito). She studied the insulator activity of retrotransposons, genomic elements present in all organisms’ genome. The study of the genetics of regulatory elements was the basis for Dr. Leronni’s background in molecular biology and her interest in gene therapy.
In 2009, Dr. Leronni was offered a fellowship as a visiting research student in the Department of Surgery at Harvard University. Here she contributed to the finding that demonstrates that mitochondria host segregated cAMP cascades with distinct functional and kinetic signatures. In this way, she began to investigate biological mechanism at a cellular level and applied her knowledge in molecular biology to carry on research in cellular biology.
In 2012, Dr. Leronni joined the University of Pittsburgh via the Department of Microbiology and Molecular Genetics as a postdoctoral associate. Under the supervision of Joseph C. Glorioso III, PhD, she gained experience in the design and generation of gene therapy vectors that can be used to deliver multiple protective genes simultaneously to neurons, with the long-term goal of using these vectors as new approaches to neurological disease.
In 2015, Dr. Leronni was recruited by Robert Friedlander, MD, as postdoctoral associate to develop novel approaches for gene therapy for Huntington’s disease (HD) and amyotrophic lateral sclerosis (ALS) and to study the basic mechanism of these diseases. One of the main objectives of her research is the creation of gene therapy vectors for HD, including, vectors targeting melatonin synthesis, which plays a protective role in the brain. Additionally, Dr. Leronni leads a research project investigating mitochondrial dysfunction in neurodegenerative disease and mitochondria signal transduction.
Specialized Areas of Interest
Biologo Professionista, Italy
Professional Organization Membership
Education & Training
- BS/MS, Biology/Molecular Genetics, Università degli Studi Aldo Moro, Bari, Italy, 2007
- Research Scholar, Cell Signaling, Harvard Medical School, 2010
- PhD, Genetics and Molecular Evolution, Università degli Studi Aldo Moro, Bari, Italy, 2011
- Postdoctoral Fellowship, Molecular Genetics/Gene Therapy, University of Pittsburgh, 2014
- Postdoctoral Fellowship, Neurodegenerative Diseases, University of Pittsburgh, 2016
Suofu Y, Li W, Jean-Alphonse FG, Jiao J, Khattar NK, Li J, Baranov SV, Leronni D, Mihalik AC, He Y, Cecon E, Wehbi VL, Kim J, Heath BE, Baranova OV, Wang X, Gable MJ, Kretz ES, Di Benedetto G, Lezon TR, Ferrando LM, Larkin TM, Sullivan M, Yablonska S, Wang J, Minnigh MB, Guillaumet G, Suzenet F, Richardson RM, Poloyac SM, Stolz DB, Jockers R, Witt-Enderby PA, Carlisle DL, Vilardaga JP, Friedlander RM. Dual role of mitochondria in producing melatonin and driving GPCR signaling to block cytochrome c release. Proc Natl Acad Sci 114(38):E7997-E8006, 2017.
Lefkimmiatis K, Leronni D, Hofer AM. The inner and outer compartments of mitochondria are sites of distinct cAMP/PKA signaling dynamics. J Cell Biol 202(3):453-62, 2013.
Marsano RM, Leronni D, D’Addabbo P, Viggiano L, Tarasco E, Caizzi R. Mosquitoes LTR Retrotransposons: A Deeper View into the Genomic Sequence of Culex Quinquefasciatus.” PLoS One 7(2): e30770, 2012.
Minervini CF, Ruggieri S, Traversa M, D'Aiuto L, Marsano RM, Leronni D, Centomani I, De Giovanni C, Viggiano L. Evidences for insulator activity of the 5'UTR of the Drosophila melanogaster LTRretrotransposon ZAM. Mol Genet Genomics 283(5):503-9, 2010.
Dr Leronni’s main project is aimed to understand the mechanism of sub-cellular localization of the Melatonin Receptor 1A (MT1). MT1 is one the two well known Melatonin-activated G protein-coupled receptors. G protein-coupled receptors (GPCRs) are classically characterized as cell surface receptors transmitting extracellular signals into cells. Dr. Robert Friedlander’s research group has recently identified functional MT1 on the mitochondrial outer membrane (MOM). Given the importance of mitochondrial homeostasis in the health and disease of all cells in the organism, it is key to understand how MT1 is targeted to the organelle and how its function is modulated.
Dr Leronni hypothesized that the MT1 generates two functional variants and that they are targeted to the plasma membrane and to the mitochondria in inverse orientation and according to two different mechanisms. Her scientific efforts have identified the post-translational modification required for the correct plasma membrane localization of the receptor, but not for its mitochondrial localization. Her goal is to identify the different mechanisms at the basis of this dual localization. Since the MT1 mitochondrial receptor plays a key role in modulating cytochrome c release, caspase activation and then the apoptotic pathway activation, understanding the biology of this receptor is key to understanding cellular function and vulnerability.