Back to list

Anna Margherita Corradi

Affiliated Researcher
Affiliated Researcher

Research Line

Neuroscience and Smart Materials

Center

NSYN@Unige Genova

Contacts

Viale Benedetto XV 3
+39 010 3538189

About

I graduated in Biological Science at the University of Genova and I performed the PhD course in Molecular and Cellular Biology at Dibit San Raffaele Scientific Institute in Milan under the supervision of Dr. Giacomo Consalez. During my PhD I developed a strong background in molecular biology, being involved in the identification of new genes with regionalized expression during development of mouse brain through PCR-based differential screening techniques (Corradi 1996, Consalez 1996, Malgaretti 1997, Mariani Corradi 1998, Consalez 1999, Gimeno 2004). Subsequently, I focused on Ebf2, an helix loop helix transcription factor isolated with this approach, and I moved to the Mouse Genetics Laboratory directed by Prof. Wolfgang Wurst in Munich to generate an Ebf2 knock out mouse. Again at Dibit I characterized the Ebf2 mutant that showed cerebellar and peripheral nervous system phenotype (Corradi 2003, Croci 2006).

Since 2002 I have worked at the Department of Experimental Medicine of the Genova University and in 2005 I had the permanent position as Assistant Professor. I concentrated on the characterization of the peripheral neuropathy of Ebf2 KO mice and on the identification of Ebf2 target genes invoved in myelination defects. In parallel, I have started to work on the molecular mechanism of neuratrasmitter release in collaboration with Prof. Fabio Benfenati by studying the Synapsin KO mice and the implication of Synapsin genes in epilepsy and autism.

In the last years, my research activity focused on another epilepsy causative gene PRRT2 (Proline Rich Transmembrane protein 2) to get insight into its fuction, I developed, in collaboration with Gaslini Institute, the generation of Induced Pluripotent Stem Cells from fibroblasts of patients carrying mutation in PRRT2 and their differentiation to excitatory neurons.

Projects

Function of the synaptic protein Prrt2 in synaptic physiology and in movement disorders

Generation of Induced pluripotent stem cells from fibroblasts of epileptic patients in collaboration with G.Gaslini Institute.

Role of Ebf2 transcription factor in peripheral nerve myelination

Involvement of Synapsin genes in epilepsy and autism

 

 

 

Selected Publications

  • Valente PL, Romei A, Fadda M, Sterlini B, Lonardoni D, Fruscione F, Castroflorio E, Michetti C, Giansante G, Valtorta F, Tsai JW, Zara F, Nieus T, Corradi A, Fassio A, Baldelli P and Benfenati F. Constitutive inactivation of the PRRT2 gene alters short-term synaptic plasticity and promotes network hyperexcitability in hippocampal neurons. Cerbral Cortex 2018. In press
  • Fruscione F, Valente P, Sterlini B, Romei A, Baldassari S, Fadda M, Prestigio C, Giansante G, Sartorelli J, Rossi P, Rubio A, Gambardella A, Nieus T, Broccoli V, Fassio A, Baldelli P, Corradi A*, Zara F*, Benfenati F*. PRRT2 controls neuronal excitability by negatively modulating Na+ channel 1.2/1.6 activity. Brain. 2018 Mar 15. * Co-senior authors.
  • Michetti C, Corradi A, Benfenati F. PRRT2, a network stability gene. . (2017). Oncotarget. 8(34):55770-55771.
  • Moruzzo D, Nobbio L, Sterlini B, Consalez GG, Benfenati F, Schenone A, Corradi A.The Transcription Factors EBF1 and EBF2 Are Positive Regulators of Myelination in Schwann Cells. (2017). Mol Neurobiol. 54(10):8117-8127.
  • Michetti C, Castroflorio E, Marchionni I, Forte N, Sterlini B, Binda F, Fruscione F, Baldelli P, Valtorta F, Zara F, Corradi A, Benfenati F. (2017). The PRRT2 knockout mouse recapitulates the neurological diseases associated with PRRT2 mutations. Neurobiol Dis. 99:66-83.
  • Valente P, Castroflorio E, Rossi P, Fadda M, Sterlini B, Cervigni RI, Prestigio C, Giovedì S, Onofri F, Mura E, Guarnieri FC, Marte A, Orlando M, Zara F, Fassio A, Valtorta F, Baldelli P, Corradi A*, Benfenati F*. (2016). PRRT2 Is a Key Component of the Ca(2+)-Dependent Neurotransmitter Release Machinery. Cell Rep. 15(1):117-31. *Co-senior authors.
  • Rossi P, Sterlini B, Castroflorio E, Marte A, Onofri F, Valtorta F, Maragliano L, Corradi A*, Benfenati F*. (20A Novel Topology of Proline-rich Transmembrane Protein 2 (PRRT2): hints for an intracellular function at the synapse. J Biol Chem. 291(12):6111-23. *Co-senior authors.
  • Brenes O, Giachello CN, Corradi AM, Ghirardi M, Montarolo PG. (2015) Synapsin knockdown is associated with decreased neurite outgrowth, functional synaptogenesis impairment, and fast high-frequency neurotransmitter release. J Neurosci Res. (10):1492-506.
  • Corradi A, Fadda M, Piton A, Patry L, Marte A, Rossi P, Cadieux-Dion M, Gauthier J, Lapointe L, Mottron L, Valtorta F, Rouleau GA, Fassio A, Benfenati F, Cossette P. (2014) SYN2 is an autism predisposing gene: loss-of-function mutations alter synaptic vesicle cycling and axon outgrowth. Hum Mol Genet. 23(1):90-103.
  • Verstegen AM, Tagliatti E, Lignani G, Marte A, Stolero T, Atias M, Corradi A, Valtorta F, Gitler D, Onofri F, Fassio A, Benfenati F. (2014) Phosphorylation of synapsin I by cyclin-dependent kinase-5 sets the ratio between the resting and recycling pools of synaptic vesicles at hippocampal synapses. J Neurosci. 34(21):7266-80.
  • Giovedí S, Corradi A, Fassio A, Benfenati F. (2014) Involvement of synaptic genes in the pathogenesis of autism spectrum disorders: the case of synapsins. Front Pediatr; 2:94. eCollection 2014. Review.
  • Gazzerro E, Baldassari S, Giacomini C, Musante V, Fruscione F, La Padula V, Biancheri R, Scarfì S, Prada V, Sotgia F, Duncan ID, Zara F, Werner HB, Lisanti MP, Nobbio L, Corradi A, Minetti C. (2012). Hyccin, the Molecule Mutated in the Leukodystrophy Hypomyelination and Congenital Cataract (HCC), Is a Neuronal Protein. PLoS One 7(3):e32180.
  • Fassio A, Patry L, Congia S, Onofri F, Piton A, Gauthier J, Pozzi D, Messa M, Defranchi E, Fadda M, Corradi A, Baldelli P, Lapointe L, St-Onge J, Meloche C, Mottron L, Valtorta F, Khoa Nguyen D, Rouleau GA, Benfenati F, Cossette P. (2011) SYN1 loss-of-function mutations in autism and partial epilepsy cause impaired synaptic function. Hum Mol Genet. 2011 Jun 15;20(12):2297-307
  • Giacomini C, La Padula V, Schenone A, Leandri M, Contestabile A, Moruzzo D, Goutebroze L, Consalez GG, Benfenati F, Corradi A. (2011) Both Schwann cell and axonal defects cause motor peripheral neuropathy in Ebf2-/- mice. Neurobiol. Dis. 42: 73-84.
  • Giachello C, Fiumara F, Giacomini C, Corradi A., Milanese C, Ghirardi M, Benfenati F And Montarolo PG (2010). MAPK/Erk-dependent phosphorylation of Synapsin mediates formation of functional synapses and short-term homosynaptic plasticity. Journal of Cell Science, vol. 123; p. 881-893. IF: 6,247
  • Corradi A, Zanardi A, Giacomini C, Onofri F, Valtorta F, Zoli M and F. Benfenati (2008). Synapsin I and Synapsin II null mice display anincreased age-dependent cognitive impairment. Journal of Cell Science, 121: 3042-51.
  • Fiumara F, Milanese C, Corradi A, Giovedì S, Leitinger G, Menegon A, Montarolo PG, Benfenati F and M. Ghirardi. (2007) Posphorylation of Synapsin domain A is required for posttetanic potentiation. Journal of Cell Science 120:3228-37.
  • Onofri F, Messa M, Metafora V, Bonanno GB, Corradi A, Bachi A, Valtorta F. and F. Benfenati (2007). Synapsin phosphorylation by Src tyrosine kinase enhances Src activity in synaptic vesicles. Journal of Biological Chemistry 282, 21: 15754-67.
  • Croci L, Chung Sh, Masserdotti G, Gianola S, Bizzocca A, Gennarini G, Corradi A., Rossi F, Hawkes R And Consalez Gg. (2006). A key role for HLH transcription factor EBF2 in Purkinje neuron migration and cerebellar cortical topography. Development. 133:2719-29.
  • Fassio A, Merlo D, Mapelli J, Menegon A, Corradi A., Mete M, Zappettini S, Bonanno Gb, Valtorta F, D'angelo E And F Benfenati. (2006). The Synapsin domain E accelerates the exoendocytotic cycle of synaptic vesicles in cerebellar Purkinje cells. Journal of Cell Science. 119.4257-68.
  • Baldelli P, Fassio A, Corradi A., Cremona O, Valtorta F And Benfenati F. (2005). Synapsin and neuroexocytosis: recent views from functional studies on Synapsin null mutant mice. Archives Italiennes De Biologie. 143 :113-126
  • Bonanomi D, Menegon A, Miccio A, Ferrari G, Corradi A., Kao Ht, Benfenati F And Valtorta F. (2005). Phosphorilation of Synapsin I by cAMP-dependent protein kinase controls synaptic vesicle dynamics in developing neurons. Journal of Neuroscience. 25 (32).7299-7308.
  • Gimeno L, Corradi A., Cobos I, Consalez Gg And Martinez S. (2004). Ezrin gene, coding for a membrane-cytoskeleton linker protein, is regionally expressed in developing mouse neuroepithelium. Gene Expression Patterns. 4 (6):749-754.
  • Corradi A., Croci L, Broccoli V, Previtali S, Wurst W, Amadio S, Maggi R, Quattrini A And Consalez Gg. (2003). Hypogonadotropic hypogonadism and peripheral neuropathy in Ebf2 -/- mice. Development. 130 (2): 401-410.
  • Consalez Gg, Cabibbo A, Corradi A., Alli C, Sardella M, Sitia R.And Fesce R. (1999). A computer-driven approach to PCR based differential screening, alternative to differential display. Bioinformatics. 15:93-105.
  • Mariani M*, Corradi A*., Baldessari D, Malgaretti N, Pozzoli O, Fesce R, Martinez S, Boncinelli E And Consalez Gg. (1998). Mab 21, the mouse homolog of a C. elegans cell-fate specification gene, participates in cerebellar, midbrain and eye development. Mechanisms of Development. 79:131-135. * The two authors contributed equally to the work.
  • Frumento G, Corradi A., Ferrara Gb And Rubartelli A. (1997). Activation-related differences in HLA class I bound peptides: presentation of IL-1 receptor antagonist derived peptide by activated but not resting CD4+ lymphocytes. Journal of Immunology.159: 5993-5999.
  • Malgaretti N, Pozzoli O, Bosetti A, Corradi A., Ciarmatori S, Panigada M, Bianchi M, Martinez S And Consalez G. (1997). Mmot1, A New Helix-Loop-Helix Transcription Factor Displaying A Sharp Expression Boundary In The Embryonic Mouse Brain. The Journal Of Biological Chemistry. 272:17632-17639
  • Consalez GG, Corradi A., Ciarmatori S, Bossolasco M, Malgaretti N, Stayton C. (1996). A New Method To Screen Clones From Differential Display Experiments Prior To Rna Studies. Trends In Genetics.12,11:455-456.
  • Corradi A., Croci L, Stayton C, Gulisano M, Boncinelli E And Consalez Gg. (1996). cDNA sequence, map and expression of the murine homolog of GTBP , a DNA mismatch repair gene. Genomics. 36:288-295.
  • Corradi A., Franzi At And A Rubartelli. (1995). Synthesis and secretion of Interleukin 1alfa and Interleukin 1 receptor antagonist during differentiation of cultured keratinocytes. Experimental Cell Research. 217: 355-362.
  • Corradi A., Bajetto A, Cozzolino F And Rubartelli A. (1993). Production and secretion of Interleukin receptor antagonist in monocytes and in keratinocytes. Cytotechnology. vol. 11.

INFORMATION NOTICE ON COOKIES

IIT's website uses the following types of cookies: browsing/session, analytics, functional and third party cookies. Users can choose whether or not to accept the use of cookies and access the website. By clicking on "Further Information", the full information notice on the types of cookies will be displayed and you will be able to choose whether or not to accept them whilst browsing on the website
Further Information
Accept and close

I numeri di IIT

L’Istituto Italiano di Tecnologia (IIT) è una fondazione di diritto privato - cfr. determinazione Corte dei Conti 23/2015 “IIT è una fondazione da inquadrare fra gli organismi di diritto pubblico con la scelta di un modello di organizzazione di diritto privato per rispondere all’esigenza di assicurare procedure più snelle nella selezione non solo nell’ambito nazionale dei collaboratori, scienziati e ricercatori ”.

IIT è sotto la vigilanza del Ministero dell'Istruzione, dell'Università e della Ricerca e del Ministero dell'Economia e delle Finanze ed è stato istituito con la Legge 326/2003. La Fondazione ha l'obiettivo di promuovere l'eccellenza nella ricerca di base e in quella applicata e di favorire lo sviluppo del sistema economico nazionale. La costruzione dei laboratori iniziata nel 2006 si è conclusa nel 2009.

Lo staff complessivo di IIT conta circa 1440 persone. L’area scientifica è rappresentata da circa l’85% del personale. Il 45% dei ricercatori proviene dall’estero: di questi, il 29% è costituito da stranieri provenienti da oltre 50 Paesi e il 16% da italiani rientrati. Oggi il personale scientifico è composto da circa 60 principal investigators, circa 110 ricercatori e tecnologi di staff, circa 350 post doc, circa 500 studenti di dottorato e borsisti, circa 130 tecnici. Oltre 330 posti su 1400 creati su fondi esterni. Età media 34 anni. 41% donne / 59 % uomini.

Nel 2015 IIT ha ricevuto finanziamenti pubblici per circa 96 milioni di euro (80% del budget), conseguendo fondi esterni per 22 milioni di euro (20% budget) provenienti da 18 progetti europei17 finanziamenti da istituzioni nazionali e internazionali, circa 60 progetti industriali

La produzione di IIT ad oggi vanta circa 6990 pubblicazioni, oltre 130 finanziamenti Europei e 11 ERC, più di 350 domande di brevetto attive, oltre 12 start up costituite e altrettante in fase di lancio. Dal 2009 l’attività scientifica è stata ulteriormente rafforzata con la creazione di dieci centri di ricerca nel territorio nazionale (a Torino, Milano, Trento, Parma, Roma, Pisa, Napoli, Lecce, Ferrara) e internazionale (MIT ed Harvard negli USA) che, unitamente al Laboratorio Centrale di Genova, sviluppano i programmi di ricerca del piano scientifico 2015-2017.

IIT: the numbers

Istituto Italiano di Tecnologia (IIT) is a public research institute that adopts the organizational model of a private law foundation. IIT is overseen by Ministero dell'Istruzione, dell'Università e della Ricerca and Ministero dell'Economia e delle Finanze (the Italian Ministries of Education, Economy and Finance).  The Institute was set up according to Italian law 326/2003 with the objective of promoting excellence in basic and applied research andfostering Italy’s economic development. Construction of the Laboratories started in 2006 and finished in 2009.

IIT has an overall staff of about 1,440 people. The scientific staff covers about 85% of the total. Out of 45% of researchers coming from abroad 29% are foreigners coming from more than 50 countries and 16% are returned Italians. The scientific staff currently consists of approximately 60 Principal Investigators110 researchers and technologists350 post-docs and 500 PhD students and grant holders and 130 technicians. External funding has allowed the creation of more than 330 positions . The average age is 34 and the gender balance proportion  is 41% female against 59% male.

In 2015 IIT received 96 million euros in public funding (accounting for 80% of its budget) and obtained 22 million euros in external funding (accounting for 20% of its budget). External funding comes from 18 European Projects, other 17 national and international competitive projects and approximately 60 industrial projects.

So far IIT accounts for: about 6990 publications, more than 130 European grants and 11 ERC grants, more than 350 patents or patent applications12 up start-ups and as many  which are about to be launched. The Institute’s scientific activity has been further strengthened since 2009 with the establishment of 11 research nodes throughout Italy (Torino, Milano, Trento, Parma, Roma, Pisa, Napoli, Lecce, Ferrara) and abroad (MIT and Harvard University, USA), which, along with the Genoa-based Central Lab, implement the research programs included in the 2015-2017 Strategic Plan.