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.