Person
Soussi-Yanicostas, Nadia
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Biography and Research Interest
Biography
Nadia Soussi-Yanicostas studied at the Université Diderot Paris VII. In 1991, she defended her science thesis at the University-Diderot Paris VII under the supervision of Gillian Butler-Browne. The contribution of his thesis work was the demonstration of the unique molecular characteristics of the human masseter muscle and the identification of molecular markers facilitating the diagnosis of several human neuromuscular diseases. Then, she carried out a first post-doctoral internship in the laboratory of Prof. François Gros at the Institut Pasteur, during which she cloned the genes of the various heavy chains of human myosin and she showed that they form a multigene complex. She then completed a second post-doctoral internship in the team of Prof. Christine Petit, at the Pasteur Institute, during which she devoted herself to the study of anosmine-1, a human protein which absence leads to Kallmann syndrome, a neurological disease associating anosmia and hypogonadotropic hypogonadism. The work she carried out during this internship and after being recruited as a CNRS researcher in 1994 was essential for understanding the role of this protein. In particular, after having established that anosmin-1 is an adhesion molecule of the extracellular matrix whose activity depends on the presence of sulphated proteoglycans, it has shown that it is also a chemoattractant factor for the neurons of the bulbs olfactory and for their axons, thus explaining the characteristic anosmia of Kallmann syndrome.
In 2004, winner of the Inserm-Avenir program, Nadia Soussi-Yanicostas created her team in the Inserm U106 unit, headed by Patricia Gaspar, at Pitié-Salpêtrière in Paris. In this laboratory, she first of all pursued the development of zebrafish (zebrafish) models of Kallmann syndrome, thus introducing this model at Pitié-Salpêtrière, with the installation of the first animal facility dedicated to the zebrafish of the site. She then established several collaborations with geneticists and neurologists at the national level and thus with her team, she studied, with the zebrafish model, the pathophysiology of several human neurodegenerative diseases; spastic paraplegias SPG11 and SPG15, spinocerebellar ataxia SCA7, Mowat-Wilson syndrome linked to the ZEB2 gene and, tauopathies.
In 2010, Nadia Soussi-Yanicostas and her team joined Inserm unit U1141, headed by Pierre Gressens, at Robert Debré Hospital, in Paris. In this new environment, she continued her research on genetic neurological diseases in zebrafish, but with a new focus; microglial cells in the brain and their involvement in several diseases of the nervous system. In particular, she and her team are studying microglial neuroinflammation and its consequences in several neurological diseases and neurodevelopmental disorders, such as epilepsy or neonatal encephalopathies. Nadia Soussi-Yanicostas is also studying the impact of different classes of pesticides on neurodevelopment. In 2017, she was promoted to Research Director at the CNRS.
Site (English): http://neurodiderot.org/index.php/soussi-en/
Site (French): http://neurodiderot.org/index.php/soussi-fr/
Current Research
The central research theme of my team is to use zebrafish embryos as in vivo tools to better understand the interactions between neurons and microglial cells in different disease contexts, such as epilepsy and childhood encephalopathy, and following environmental insults, such as pesticide poisoning. Specifically, we use a multidisciplinary approach, combining zebrafish mutants, transgenic technologies, in vivo calcium imaging, electrophysiology, behavioural studies, and classic molecular biology methods of protein and RNA analysis, to: (i) precisely characterize the spectrum of microglia activities induced by different types of neuron dysfunctions resulting from either disease or poisoning, and (ii) better understanding the consequences of these microglia activities (neuro-inflammation and/or neuro-protection) on subsequent neuron physiology. Currently, the research activity of my team is focused on two main research projects. The first aims at investigating the activity of microglia in different genetic epilepsy contexts in zebrafish (using mutant lines scn1Lab-/-, depdc5-/-, gabra1-/- and gabrg2-/-, four genes that have been found mutated in human Dravet syndrome childhood epilepsy) and also better understand the consequences of this microglia activity on subsequent brain functioning and neuron excitability. In line with this research theme, using diisopropylfluorophodphate (DFP), a mildly toxic organophosphorus (OP) compound analogous to warfare agents Sarin and Soman, we are also investigating the mechanism underlying the epileptogenic effect of OPs and seek identifying effective countermeasures. Our second project is in line with the recent demonstration in our laboratory that succinate dehydrogenase inhibitor (SDHI) molecules, the most widely used fungicides in agriculture practices today, are not fungus-specific and efficient inhibit SDH activity in honey bees, lumbrics and human cells. In our team we are studying the role of three SDHIs, which has never been estimated in in vivo models, on neurodevelopment and neurobehavior.
Site (English): http://neurodiderot.org/index.php/soussi-en/
Site (French): http://neurodiderot.org/index.php/soussi-fr/
Keywords: Epilepsy; Microglia; Zebrafish; Neuroprotection; Dravet syndrome; Encephalopathies; Pesticides; Synapses; Tauopathies; Neuro-inflammation; Tau; Abeta; Behaviour; Organophosphorus, Calcium imaging; Autism; Genetic models of Epilepsy in zebrafish.
Nadia Soussi-Yanicostas studied at the Université Diderot Paris VII. In 1991, she defended her science thesis at the University-Diderot Paris VII under the supervision of Gillian Butler-Browne. The contribution of his thesis work was the demonstration of the unique molecular characteristics of the human masseter muscle and the identification of molecular markers facilitating the diagnosis of several human neuromuscular diseases. Then, she carried out a first post-doctoral internship in the laboratory of Prof. François Gros at the Institut Pasteur, during which she cloned the genes of the various heavy chains of human myosin and she showed that they form a multigene complex. She then completed a second post-doctoral internship in the team of Prof. Christine Petit, at the Pasteur Institute, during which she devoted herself to the study of anosmine-1, a human protein which absence leads to Kallmann syndrome, a neurological disease associating anosmia and hypogonadotropic hypogonadism. The work she carried out during this internship and after being recruited as a CNRS researcher in 1994 was essential for understanding the role of this protein. In particular, after having established that anosmin-1 is an adhesion molecule of the extracellular matrix whose activity depends on the presence of sulphated proteoglycans, it has shown that it is also a chemoattractant factor for the neurons of the bulbs olfactory and for their axons, thus explaining the characteristic anosmia of Kallmann syndrome.
In 2004, winner of the Inserm-Avenir program, Nadia Soussi-Yanicostas created her team in the Inserm U106 unit, headed by Patricia Gaspar, at Pitié-Salpêtrière in Paris. In this laboratory, she first of all pursued the development of zebrafish (zebrafish) models of Kallmann syndrome, thus introducing this model at Pitié-Salpêtrière, with the installation of the first animal facility dedicated to the zebrafish of the site. She then established several collaborations with geneticists and neurologists at the national level and thus with her team, she studied, with the zebrafish model, the pathophysiology of several human neurodegenerative diseases; spastic paraplegias SPG11 and SPG15, spinocerebellar ataxia SCA7, Mowat-Wilson syndrome linked to the ZEB2 gene and, tauopathies.
In 2010, Nadia Soussi-Yanicostas and her team joined Inserm unit U1141, headed by Pierre Gressens, at Robert Debré Hospital, in Paris. In this new environment, she continued her research on genetic neurological diseases in zebrafish, but with a new focus; microglial cells in the brain and their involvement in several diseases of the nervous system. In particular, she and her team are studying microglial neuroinflammation and its consequences in several neurological diseases and neurodevelopmental disorders, such as epilepsy or neonatal encephalopathies. Nadia Soussi-Yanicostas is also studying the impact of different classes of pesticides on neurodevelopment. In 2017, she was promoted to Research Director at the CNRS.
Site (English): http://neurodiderot.org/index.php/soussi-en/
Site (French): http://neurodiderot.org/index.php/soussi-fr/
Current Research
The central research theme of my team is to use zebrafish embryos as in vivo tools to better understand the interactions between neurons and microglial cells in different disease contexts, such as epilepsy and childhood encephalopathy, and following environmental insults, such as pesticide poisoning. Specifically, we use a multidisciplinary approach, combining zebrafish mutants, transgenic technologies, in vivo calcium imaging, electrophysiology, behavioural studies, and classic molecular biology methods of protein and RNA analysis, to: (i) precisely characterize the spectrum of microglia activities induced by different types of neuron dysfunctions resulting from either disease or poisoning, and (ii) better understanding the consequences of these microglia activities (neuro-inflammation and/or neuro-protection) on subsequent neuron physiology. Currently, the research activity of my team is focused on two main research projects. The first aims at investigating the activity of microglia in different genetic epilepsy contexts in zebrafish (using mutant lines scn1Lab-/-, depdc5-/-, gabra1-/- and gabrg2-/-, four genes that have been found mutated in human Dravet syndrome childhood epilepsy) and also better understand the consequences of this microglia activity on subsequent brain functioning and neuron excitability. In line with this research theme, using diisopropylfluorophodphate (DFP), a mildly toxic organophosphorus (OP) compound analogous to warfare agents Sarin and Soman, we are also investigating the mechanism underlying the epileptogenic effect of OPs and seek identifying effective countermeasures. Our second project is in line with the recent demonstration in our laboratory that succinate dehydrogenase inhibitor (SDHI) molecules, the most widely used fungicides in agriculture practices today, are not fungus-specific and efficient inhibit SDH activity in honey bees, lumbrics and human cells. In our team we are studying the role of three SDHIs, which has never been estimated in in vivo models, on neurodevelopment and neurobehavior.
Site (English): http://neurodiderot.org/index.php/soussi-en/
Site (French): http://neurodiderot.org/index.php/soussi-fr/
Keywords: Epilepsy; Microglia; Zebrafish; Neuroprotection; Dravet syndrome; Encephalopathies; Pesticides; Synapses; Tauopathies; Neuro-inflammation; Tau; Abeta; Behaviour; Organophosphorus, Calcium imaging; Autism; Genetic models of Epilepsy in zebrafish.
Non-Zebrafish Publications
Igert, Stéphane Auvin, Rahma Hassan-Abdi, Nadia Soussi-Yanicostas, et al.
Time-sequential Neuroinflammatory Response After Organophosphate-induced Status Epilepticus
DOI: 10.21203/rs.3.rs-72760/v1.
Mairesse J, et al. O Baud*, N Soussi-Yanicostas*. * last co-authors.
Oxytocin receptor agonist reduces perinatal brain damage by targeting microglia.
Glia. 2019;67(2):345-359. doi: 10.1002/glia.23546.
Van Steenwinckel J, et al. Soussi-Yanicostas N, Fleiss B, Gressens P
Decreased microglial Wnt/β-catenin signalling drives microglial pro-inflammatory activation in the developing brain.
Brain. 2019;142(12):3806-3833. doi:10.1093/brain/awz319.
Auvin S, Jeljeli M, Desnous B, Soussi-Yanicostas N, Dournaud P, Sterkers G.
Altered vaccine-induced immunity in children with Dravet syndrome.
Epilepsia. 2018;59(4):e45-e50. doi:10.1111/epi.14038.
Ghoumid J, et al., and Soussi-Yanicostas N, Giurgea I.
ZEB2 zinc-finger missense mutations lead to hypomorphic alleles and a mild Mowat-Wilson syndrome.
Hum Mol Genet. 2013, 1;22(13):2652-61. doi: 10.1093/hmg/ddt114.
Ayari B, Landoulsi A, Soussi-Yanicostas N.
Localization and characterization of kal 1.a and kal 1.b in the brain of adult zebrafish (Danio rerio).
Brain Res Bull. 2012, Jul 1;88(4):345-53. doi: 10.1016/j.brainresbull.2012.03.006.
García-González D, Clemente D, Coelho M, Esteban PF, Soussi-Yanicostas N, de Castro F.
Dynamic roles of FGF-2 and Anosmin-1 in the migration of neuronal precursors from the subventricular zone during pre- and postnatal development.
Exp Neurol. 2010 Apr;222(2):285-95. doi: 10.1016/j.expneurol.2010.01.006.
Puverel S, Nakatani H, Parras C, Soussi-Yanicostas N.
Prokineticin receptor 2 expression identifies migrating neuroblasts and their subventricular zone transient-amplifying progenitors in adult mice.
J Comp Neurol. 2009 Jan 10;512(2):232-42. doi: 10.1089/neu.2009.0972.
Bribián A, Esteban PF, Clemente D, Soussi-Yanicostas N, Thomas JL, Zalc B, de Castro F.
A novel role for anosmin-1 in the adhesion and migration of oligodendrocyte precursors.
Dev Neurobiol. 2008 Nov;68(13):1503-16. doi: 10.1002/dneu.20678.
Clemente D, Esteban PF, Del Valle I, Bribián A, Soussi-Yanicostas N, Silva A, De Castro F.
Expression pattern of Anosmin-1 during pre- and postnatal rat brain development.
Dev Dyn. 2008 Sep;237(9):2518-28. doi: 10.1002/dvdy.21659.
Ayari B, Soussi-Yanicostas N.
FGFR1 and anosmin-1 underlying genetically distinct forms of Kallmann syndrome are co-expressed and interact in olfactory bulbs.
Dev Genes Evol. 2007 Feb;217(2):169-75. doi: 10.1007/s00427-006-0125-0.
Bribián A, Barallobre MJ, Soussi-Yanicostas N, de Castro F.
Anosmin-1 modulates the FGF-2-dependent migration of oligodendrocyte precursors in the developing optic nerve.
Mol Cell Neurosci. 2006 Sep;33(1):2-14. doi: 10.1016/j.mcn.2006.05.009.
Dodé C, Levilliers J, Dupont JM, De Paepe A, Le Dû N, Soussi-Yanicostas N, et al.
Loss-of-function mutations in FGFR1 cause autosomal dominant Kallmann syndrome.
Nat Genet. 2003 Apr;33(4):463-5. doi: 10.1038/ng1122.
Dellovade TL, Hardelin JP, Soussi-Yanicostas N, et al.
Anosmin-1 immunoreactivity during embryogenesis in a primitive eutherian mammal.
Brain Res Dev Brain Res. 2003 Feb 16;140(2):157-67. doi: 10.1016/s0165-3806(02)00544-8.
Soussi-Yanicostas N, et al.
Anosmin-1, defective in the X-linked form of Kallmann syndrome, promotes axonal branch formation from olfactory bulb output neurons.
Cell. 2002 Apr 19;109(2):217-28.
Hardelin JP, Julliard AK, Moniot B, Soussi-Yanicostas N, et al.
Anosmin-1 is a regionally restricted component of basement membranes and interstitial matrices during organogenesis: implications for the developmental anomalies of X chromosome-linked Kallmann syndrome.
Dev Dyn. 1999 May;215(1):26-44.
Soussi-Yanicostas N, et al.
Anosmin-1 underlying the X chromosome-linked Kallmann syndrome is an adhesion molecule that can modulate neurite growth in a cell-type specific manner.
J Cell Sci. 1998 Oct;111 ( Pt 19):2953-65. PMID: 9730987.
Soussi-Yanicostas N, et al.
Initial characterization of anosmin-1, a putative extracellular matrix protein synthesized by definite neuronal cell populations in the central nervous system.
J Cell Sci. 1996 Jul;109 ( Pt 7):1749-57. PMID: 8832397.
Hamida CB, Soussi-Yanicostas N, et al.
Expression of myosin isoforms and of desmin, vimentin and titin in Tunisian Duchenne-like autosomal recessive muscular dystrophy.
J Neurol Sci. 1994 May;123(1-2):114-21. doi: 10.1016/0022-510x(94)90212-7.
Ben Hamida C, Soussi-Yanicostas N, Butler-Browne GS, Bejaoui K, Hentati F, Ben Hamida.
Biochemical and immunocytochemical analysis in chronic proximal spinal muscular atrophy.
Muscle Nerve. 1994 Apr;17(4):400-10. doi: 10.1002/mus.880170407.
Soussi-Yanicostas N, Whalen RG, Petit C.
Five skeletal myosin heavy chain genes are organized as a multigene complex in the human genome.
Hum Mol Genet. 1993 May;2(5):563-9. doi: 10.1093/hmg/2.5.563.
Soussi-Yanicostas N, et al.
Evolution of muscle specific proteins in Werdnig-Hoffman's disease.
J Neurol Sci. 1992 May;109(1):111-20.
Soussi-Yanicostas N, Butler-Browne GS.
Transcription of the embryonic myosin light chain gene is restricted to type II muscle fibers in human adult masseter.
Dev Biol. 1991 Oct;147(2):374-80. doi: 10.1016/0012-1606(91)90295-e.
Soussi-Yanicostas N, et al.
Modification in the expression and localization of contractile and cytoskeletal proteins in Schwartz-Jampel syndrome.
J Neurol Sci. 1991 Jul;104(1):64-73.
Rotter M, Zimmerman K, Poustka A, Soussi-Yanicostas N, Starzinski-Powitz A.
The human embryonic myosin alkali light chain gene: use of alternative promoters and 3' non-coding regions.
Nucleic Acids Res. 1991 Apr 11;19(7):1497-504. doi: 10.1093/nar/19.7.1497.
Laurent-Winter C, Soussi-Yanicostas N, Butler-Browne GS.
Biphasic expression of slow myosin light chains and slow tropomyosin isoforms during the development of the human quadriceps muscle.
FEBS Lett. 1991 Mar 25;280(2):292-6. doi: 10.1016/0014-5793(91)80315-t.
Soussi-Yanicostas N, et al.
Distinct contractile protein profile in congenital myotonic dystrophy and X-linked myotubular myopathy.
Neuromuscul Disord. 1991;1(2):103-11.
Soussi-Yanicostas N, et al.
Transition of myosin isozymes during development of human masseter muscle. Persistence of developmental isoforms during postnatal stage.
Development. 1990 Feb;108(2):239-49. PMID: 2140978.
Yanicostas C, Soussi-Yanicostas N, El-Khoury R, Bénit P, Rustin P.
Developmental aspects of respiratory chain from fetus to infancy.
Semin Fetal Neonatal Med. 2011 Aug;16(4):175-80. doi: 10.1016/j.siny.2011.05.005.
Hardelin JP, Soussi-Yanicostas N, Ardouin O, Levilliers J, Petit C.
Kallmann syndrome.
Adv Otorhinolaryngol. 2000; 56:268-74.
Hardelin, J.-P., Soussi-Yanicostas, N., et al.
Molecular approach to the pathogenesis of renal anomalies in the Kallmann de Morsier syndrome and in the branchio-oto-renal syndrome.
Advances in Nephrology 1998, 28, 419-428.
Hardelin JP, Soussi-Yanicostas N, et al.
Molecular approach to the pathogenesis of renal anomalies in Kallmann's syndrome and in the branchio-oto-renal syndrome.
Adv Nephrol Necker Hosp. 1998;28:419-28.
Soussi-Yanicostas N., et al.
Approche moléculaire de la pathogénie d’un déficit héréditaire de l’olfaction : le syndrome de Morsier lié au chromosome X.
Annales de l’Institut Pasteur 1995, 6, 282-291.
Soussi-Yanicostas N.
L’ontogenèse musculaire : De l’induction mésodermique à la formation du sarcomère.
Bulletin de l’Institut Pasteur 1991, 89, 255-295.
Soussi-Yanicostas N., Breuer E., Dang, D., Butler-Browne G.
The masseter, a very specialized muscle.
Muscle and Motility 1990, 2, 63-70.
Coelho, M, Soussi-Yanicostas N, de Castro, F.
The formation of the rostral migratory stream: New insights in its molecular basis.
CHEMICAL SENSES 2006, Volume: 31, Issue: 8, Pages: E25.
Hardelin J-P., Soussi-Yanicostas N., Ardouin O., Levilliers J., Petit C.
Kallmann syndrome.
In Advances in Oto-Rhino-Laryngology 2000 , K. Kitamura and K.P. Steel, eds. (Basal, Karger, SA). 56, 268-274.
Hardelin J-P., Levilliers J., Soussi-Yanicostas N., et al.
Approche moléculaire de la pathogénie des anomalies rénales dans le syndrome de Kallmann de Morsier et dans le syndrome branchio-oto-rénal.
Actualités Néphrologiques 1998, Jean Hamburger, Grünefeld JP, Bach JF, & Kreis H, eds. Médecine-Sciences Flammarion. 333-340.
Soussi-Yanicostas N. Colloque recherche FIRENDO 2019- ‘Apport du modèle poisson zèbre (zebrafish) à l’étude des maladies rares’ ; Livret : Livret_bilan_Colloque_Recherche_2019_.pdf.
Lien : http://www.firendo.fr/fileadmin/user_upload/JAF2019/Livret_bilan_Colloque_Recherche_2019_.pdf
Van Steenwinckel, J ; et al. Soussi-Yanicostas N, HFleiss, B ; Gressens, P.
Loss of the Wnt pathway in microglia drives pro-inflammatory activation leading to perinatal white matter injury.
GLIA 2017, Volume: 65, Pages: E459-E459, Supplement: 1.
Gressens, P ; et al., and Soussi-Yanicostas N.
Microglial WNT signaling inhibition promotes microglia activation and oligodendrocyte maturation blockade
JOURNAL OF NEUROCHEMISTRY 2015, Volume: 134, Pages: 122-122, Supplement: 1, Special issue:S1.
Fleiss, B; et al. ; Soussi-Yanicostas, N; Gressens, P.
Microglial Wnt signaling inhibition promotes microglia activation and oligodendrocyte maturation blockade
GLIA 2015, Volume: 63 Pages: E367-E368 Supplement: 1 Meeting Abstract: T12-16B.
Patents
Soussi-Yanicostas N, Yanicostas C, Alavi-Naini MS.
International patent (deposit number: PCT/EP2012106523, 2011). Materials and methods for the treatment of tauopathies. This patent was extended to the United States in June 2016 (N° de dépôt : 15/196,180).
Papy-Garcia D, Huyn B, Soussi-Yanicostas N, et al.
European patent (deposit number: 12300005414.0-2107, 2012). Method of diagnosis, pronostic or treatment of neurodegenerative diseases. This patent was extended to the United States (01/06/2016, Number 15/196,180), Depositor: SATT Ile-de-France Innov.
Chritine Petit, Nadia Soussi-Yanicostas, et coll. (1998). Use of the KAL protein and treatment with the KAL protein in treatment of neural injury. Brevet déposé par l’Institut Pasteur (N°761,136).