ENS - Départment de biologie

Dmitry RINBERG Sensory (olfactory) coding from behavioral perspective

Patricia Mangeny — 2026-10-22T14:30:00Z

16h30

Le cours-séminaire de Dmitry Rinberg (Department of Neuroscience, NYU Grossman School of Medicine) aura lieu dans la salle Favard, IBENS 46 rue d'Ulm 75005 Paris

Two of the most fundamental questions of sensory neuroscience are : 1) how is stimulus information represented by neuronal activity ? and 2) what features of this activity are read out to guide behavior ? The first question has been the subject of a large body of work across different sensory modalities. The second question remains a significant challenge, since one needs to establish a causal link between neuronal activity and behavior.

In olfaction, it has been proposed that information about odors is encoded in spatial distribution of receptor activation and the next level mitral/tufted cells, as well as in their relative timing and synchrony. However, the role of different features of neural activity in guiding behavior remains unknown. Using mouse olfaction as a model system, I will present our work on developing both technological and conceptual approaches to study sensory coding by perturbing neural activity at different levels of information processing during sensory driven behavioral tasks. We will first ask the questions about psychophysical limits of the readability of different features of the neural code, and, second, how to quantify their behavioral relevance.

Prof. Hananeh FONOUDI Understanding complex cardiac disorders by modeling cellular crosstalk with human organoids

Patricia Mangeny — 2026-10-19T09:00:00Z

11h
Le séminaire de la Prof. Hananeh Fonoudi (Emory University, USA) aura lieu dans la salle Favard, IBENS 46 rue d'Ulm 75005 Paris

- 2026 / Séminaire de l'IBENS

Dmitry RINBERG Introduction to olfaction

Patricia Mangeny — 2026-10-15T14:30:00Z

16h30

Le cours-séminaire de Dmitry Rinberg (Department of Neuroscience, NYU Grossman School of Medicine ) aura lieu dans la salle Favard, IBENS 46 rue d'Ulm 75005 Paris

Olfaction is the main sense used by most animals to interact with the environment. It is probably the oldest evolutionary senses. From bacteria to humans, life organisms extract information from chemical world around them. An anatomical organization of olfactory system is similar from insect to mammals. Here I will describe the basic olfactory biology and information processing in the mammalian olfactory system : from receptors to perception. I will discuss unsolved fundamental questions in the field.

Nathalie ROCHEFORT Neuromodulation of vision in SYNGAP1-related disorder

Patricia Mangeny — 2026-10-12T09:00:00Z

11h
Le séminaire de Nathalie Rochefort (University of Edinburgh, UK) aura lieu dans la salle Favard, IBENS 46 rue d'Ulm 75005 Paris

- 2026 / Séminaire de l'IBENS

Francisco ÚBEDA DE TORRES On the origin of PRDM9-guided recombination hotspots

Patricia Mangeny — 2026-10-09T10:00:00Z

12h

Le séminaire de Francisco Úbeda de Torres (School of Biological Sciences at Royal Holloway, University of London) aura lieu dans la salle Favard, IBENS 46 rue d'Ulm 75005 Paris

Across vertebrates, meiotic recombination is guided either by the protein PRDM9, which targets DNA sequences that are gradually destroyed, or by non-PRDM9 mechanisms that act in open chromatin without sequence specificity. Why a self-destructive mechanism evolves alongside a durable alternative remains unresolved. Using a population genetic model, we show that PRDM9-guided hotspots are generally disfavored because they generate fewer binding events and thus fewer crossovers needed to produce viable gametes. However, they can be favored when they promote simultaneous binding of both homologous chromosomes (symmetric binding), which more often produces crossovers. The evolutionary fate of PRDM9 thus reflects a trade-off between reduced binding and enhanced symmetric binding, explaining the diversity and evolutionary turnover of recombination mechanisms observed across vertebrates today.

Léa HUILIO Régulations de CIRBP en réponse aux stress liés à l'infection bactérienne

Patricia Mangeny — 2026-10-06T12:00:00Z

14h

La soutenance de thèse de Léa Huilio (sous la direction d'Alice Lebreton, IBENS) aura lieu dans la salle Jean Jaurès, 29 rue d'Ulm 75005 Paris

Résumé :
Au cours de l'infection de cellules humaines par la bactérie pathogène alimentaire Listeria monocytogenes, l'expression des gènes de l'hôte est remaniée par différents mécanismes, notamment par épissage alternatif. Ce manuscrit porte sur l'étude d'un facteur de réponse au stress régulé par ce mécanisme, la protéine de liaison à l'ARN CIRBP (Cold-inducible RNA Binding Protein, Protéine de liaison à l'ARN induite par le froid), dont l'expression bascule vers un isoforme alternatif au cours de l'infection sous l'effet de la listériolysine O, une toxine bactérienne qui forme des pores dans la membrane plasmique et qui affecte l'activité de la kinase CLK1, régulatrice des facteurs d'épissage SRSF. Cette bascule d'épissage conduit à un déséquilibre entre deux isoformes protéiques de CIRBP, CIRBP-201 et CIRBP-210, qui ne diffèrent que de cinq acides aminés en région C-terminale. L'activité cytolytique de la LLO conduit par ailleurs au relargage de CIRBP dans le milieu extracellulaire. Afin de déterminer si les deux isoformes protéiques de CIRBP se comportent différemment au cours de l'infection, j'ai comparé leur localisation subcellulaire, leur capacité de sécrétion, leur devenir au sein des granules de stress. Aucune différence marquée n'a été observée entre les deux isoformes. Ces résultats suggèrent que la bascule d'épissage observée au cours de l'infection viserait principalement à produire un transcrit instable, réduisant ainsi la quantité totale de CIRBP produite, plutôt qu'à générer deux protéines aux propriétés distinctes. Sur le plan fonctionnel, mes travaux montrent que CIRBP favorise l'infection des cellules épithéliales par Listeria monocytogenes, un effet généralisable à cinq autres espèces bactériennes. Afin de déterminer à quelle étape du cycle infectieux CIRBP agit, j'ai évalué son impact sur l'adhésion des bactéries à la surface cellulaire, leur internalisation, leur croissance intracellulaire, ainsi que leur échappement à l'autophagie. Cette étude a révélé que c'est principalement l'adhésion bactérienne qui est modulée par CIRBP, les autres étapes du cycle infectieux n'étant pas affectées. Cette fonction pro-adhésive repose sur la forme extracellulaire de la protéine plutôt que sur son activité intracellulaire de protéine de liaison à l'ARN, et se révèle indépendante de l'isoforme exprimé. Les récepteurs impliqués dans cette interaction ainsi que les mécanismes moléculaires sous-jacents restent à identifier. Mes travaux identifient ainsi CIRBP comme un nouvel acteur pro-bactérien de l'infection par Listeria monocytogenes, agissant spécifiquement comme modulateur de l'étape d'adhésion par voie paracrine.

Harmit MALIK Genetic conflicts drive the unexpected rapid evolution of essential chromatin proteins

Patricia Mangeny — 2026-10-02T10:00:00Z

12h

Le séminaire d'Harmit Malik (Fred Hutchinson Institute in Seattle, USA) aura lieu dans la salle Favard, IBENS 46 rue d'Ulm 75005 Paris

Harmit Singh Malik is an evolutionary biologist renowned for uncovering how genetic conflicts and evolutionary “arms races” between genomes shape fundamental cellular processes and host–pathogen interactions. He is a Howard Hughes Medical Institute Investigator and professor in the Basic Sciences Division at Fred Hutchinson Cancer Center in Seattle, where he leads a research program centered on the causes and consequences of genetic conflict. Malik is best known for helping to develop the centromere-drive model, which explains how “selfish” centromeres can bias their transmission during female meiosis, thereby driving the rapid evolution of centromeric DNA and its associated proteins. His lab has also recently adapted these ideas to the unexplained rapid evolution of protamine genes in animals, suggesting that they too are rapidly evolving to suppress meiotic drive, but in male meiosis. Across these projects, his group uses evolution-guided approaches to identify rapidly evolving genes, link signatures of positive selection to mechanisms, and illuminate how conflicts between genes influence genome evolution and the origin of new species.

Faadil MUSTUN Des sifflements à la communication : vers une compréhension computationnelle des signaux acoustiques des dauphins

Patricia Mangeny — 2026-10-01T12:00:00Z

14h
La soutenance de thèse de Faadil Mustun (IBENS, équipe Sumbre) aura lieu dans la salle Favard, IBENS 46 rue d'Ulm 75005 Paris

- 2026 / Soutenance de thèse

Dr. Itai A. TOKER How do brains evolve ? Probing the evolution of neurodifferentiation and neural function throughout the brain in the tractable Nematoda model phylum

Patricia Mangeny — 2026-09-30T09:00:00Z

11h
Le séminaire du Dr. Itai A. Toker (Columbia University, NY) aura lieu dans la salle Favard, IBENS 46 rue d'Ulm 75005 Paris

- 2026 / Séminaire de l'IBENS

Julia DORIA Mécanismes moléculaires et pharmacologie des récepteurs GluD, une famille atypique de récepteurs ionotropiques au glutamate.

Patricia Mangeny — 2026-09-29T12:00:00Z

14h

La soutenance de thèse de Julia Doria (sous la direction de Laetitia Mony et Pierre Paoletti) aura lieu dans la salle Favard, IBENS 46 rue d'Ulm 75005 Paris

Molecular mechanisms and pharmacology of GluD receptors, an atypical family of ionotropic glutamate receptors
Ionotropic glutamate receptors (iGluRs) are a well-characterized family of ligand-gated ion channels typically defined by two main features : glutamate binding and ligand-gated ion channel activity. However, in the Delta subclass of iGluRs, GluD1 receptors display highly atypical properties. Indeed, GluD1 receptors do not bind glutamate but rather D-serine and GABA, which does not appear to trigger channel opening under classical electrophysiolocal recording conditions.
Growing evidence supports important physiological roles in synapse formation and inhibitory plasticity of GluD1 receptors, as well as their involvement in pathologies like schizophrenia. Yet, the molecular basis of their signaling remains poorly understood. In particular, their intrinsic electrical silence makes their study in native systems challenging. As a result, GluD1 receptors have so far escaped comprehensive pharmacological and biophysical characterization.
To address this gap, we developed several tools – (i) a mutation of GluD1 pore to create constitutively open channels (“Lurcher” mutant) and (ii) voltage-clamp fluorometry, a fluorescence-based method allowing real-time monitoring of receptor conformational changes – to investigate GluD1 conformational changes and its mechanisms of signaling.
We found out that, although they both bind to the same binding-site, GABA and D-serine appear to induce different gating mechanisms. Indeed, voltage-clamp fluorometry experiments revealed distinct conformational changes induced by GABA and D-serine. We furthermore characterized GluD1 calcium binding site and showed a differential role of this allosteric modulation on GABA and D-serine. Finally, we demonstrated the key role of LBD dimer interfaces, especially of GluD-specific loop located at the level of the LBD lower lobe, in the control of GluD1 gating and ligand sensitivity.
This discovery of differing mechanisms induced by two orthosteric agonists suggests distinct signaling mechanisms, with potential strong implications for neuronal physiology. Hence, by providing new insights into pharmacology and molecular mechanisms of GluD1 receptors, this study should lead to a better understanding of GluD1 physiological roles in the brain.