ENS - Départment de biologie

Multiple functions of cerebello-thalamic neurons in learning and offline consolidation of a motor skill in mice

Tommaso VILLA — 2026-06-11T16:05:53Z

Authors
Andrés Pablo Varani, Caroline Mailhes-Hamon, Romain W Sala, Marie Sarraudy, Sarah Fouda, Jimena L Frontera, Clément Léna^#, Daniela Popa^#

Abstract

Motor skill learning is a complex and gradual process that involves the cortex and basal ganglia, both crucial for the acquisition and long-term retention of skills. The cerebellum, which rapidly learns to adjust the movement, connects to the motor cortex and the striatum primarily via the ventral and intralaminar thalamus, respectively. Here, we evaluated the contribution of cerebellar neurons projecting to these thalamic nuclei in a skilled locomotion task in mice. Using a targeted chemogenetic inhibition that preserves the motor abilities, we found that cerebellar nuclei neurons projecting to the intralaminar thalamus contribute to learning and expression, while cerebellar nuclei neurons projecting to the ventral thalamus contribute to offline consolidation. Asymptotic performance, however, required each type of neurons. Thus, our results show that cerebellar neurons belonging to two parallel cerebello-thalamic pathways play distinct, but complementary, roles functioning on different timescales and both necessary for motor skill learning.

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Elife. 2026 Apr 22:13:RP102813. doi : 10.7554/eLife.102813.

Chris Bowler, élu membre de la Royal Society, l'académie nationale des sciences du Royaume-Uni

Tommaso VILLA — 2026-06-03T09:55:24Z

La Royal Society est une association autonome qui regroupe bon nombre des scientifiques, ingénieurs et technologues les plus éminents au monde.

Lien vers l'annonce de la Royal Society

Lien vers le profil de Chris Bowler sur le site web de la Royal Society

Appel à candidature : Chaire de Professeur-e Junior de l'Inserm “Génération et Régénération Cellulaire et Tissulaire”

Tommaso VILLA — 2026-03-27T14:28:09Z

L'Inserm lance un appel à candidatures pour un poste de Chaire de Professeur·e Junior intitulée "Génération et Régénération Cellulaire et Tissulaire", dont l'activité se déroulera à l'Institut de Biologie de l'École Normale Supérieure (IBENS), Université Paris Sciences et Lettres, au sein de la section Biologie du Développement.

Ce recrutement, basé sur des projets de recherche et d'enseignement, s'adresse à des chercheurs présentant un fort potentiel pour diriger et animer des équipes de recherche ainsi que pour participer à des projets nationaux, européens ou internationaux. Le poste est proposé dans le cadre d'un contrat à durée déterminée (CDD) de 4 ans, en vue d'une titularisation au sein du corps des Directeurs de Recherche de l'Inserm à l'issue du contrat. Le poste comprend un salaire proportionnel à l'expérience en recherche ainsi qu'un fonds de démarrage de 200 K€.

Le(a) candidat(e) retenu(e) devra mettre en place un projet scientifique ambitieux allant au-delà de la biologie du développement traditionnelle et de la recherche sur les cellules souches, afin de comprendre les mécanismes fondamentaux qui régissent la structuration des tissus et la morphogenèse, ouvrant ainsi de nouvelles perspectives pour la régénération cellulaire et tissulaire, avec des implications importantes pour la santé humaine.

Le(a) candidat(e) retenu(e) participera activement au programme d'enseignement du Master en Sciences de la Vie-IMALIS (Master interdisciplinaire en Sciences de la Vie) de l'Université PSL et s'engagera dans le programme L3 du Département de Biologie de l'ENS ainsi que dans le programme Médecine-Sciences, géré conjointement par l'ENS-PSL, l'Institut Curie et l'Institut Pasteur. Ces initiatives visent à former de futurs médecins-chercheurs de très haut niveau, capables de mener des recherches biomédicales innovantes.

Les candidatures peuvent être déposées en ligne depuis le portail EVA à partir du 8 avril 2026

Plus d'informations sur l'offre d'emploi

Date limite de candidature : 2 Septembre 2026

Replacing car-dedicated space with green spaces : an assessment of the mortality benefits in Paris

Tommaso VILLA — 2026-03-10T08:43:08Z

Abstract

Background
Increasing urban vegetation coverage is associated with improved human health and well-being, reduced environmental impact of cities and enhanced urban resilience to climate change.
Objectives
To support evidence-based urban planning, this study quantifies the mortality benefits, equity implications and cost-benefit ratio of several scenarios of green space development in Paris by 2040, including the replacement of car-dedicated surfaces with green spaces and a best-case scenario.
Methods
This quantitative health impact assessment is based on estimated changes in the Normalized Difference Vegetation Index (NDVI), obtained through the estimation of the dynamic effects over time using a Difference-in-Differences approach based on previous public greening interventions, and on an exposure-response relationship linking NDVI and all-cause mortality. It was conducted at the sub-municipal level (IRIS) and incorporates a social deprivation index to assess health equity implications. Vegetation costs are drawn from a previous French study estimating urban soil restoration prices.
Results
Replacing surplus on-street parking and 20% of street space with vegetation could reduce all-cause mortality by around 0.8%, while reaching 15% of vegetation coverage in each IRIS could prevent around 3% of deaths yearly in Paris as early as 2040. For all scenarios, these benefits were approximately equally distributed across deprivation levels. Predicted monetised health benefits outweigh intervention costs by 2035, with further impacts representing net gain.
Conclusion
In conclusion, greening interventions targeting car-dedicated space in Paris would equitably improve health while supporting more sustainable and resilient cities.

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Environ Res. 2026 Mar 4:297:124157. doi : 10.1016/j.envres.2026.124157.

Fluctuating Growth Rates Link Turnover and Unevenness in Species-Rich Communities

Tommaso VILLA — 2026-02-20T16:00:14Z

Abstract

The maintenance of diversity, the 'commonness of rarity', and compositional turnover are ubiquitous features of species-rich communities. Through a minimal model, we consider how these features reflect the interplay between environmental stochasticity, intra- and interspecific competition, and dispersal. We show that, even if species have the same time-average fitness, fluctuations tend to drive the community towards ever-growing unevenness and species extinctions, but self-limitation and/or dispersal allow species-rich states to be sustained. Species abundance-distributions vary systematically in a Buffering-Stabilisation parameter plane that describes the relative strength of the underlying ecological processes, and cover different empirically relevant power-law and unimodal shapes. A model describing the effective dynamics of a focal species relates static abundance distributions with turnover dynamics, also when species have different mean fitness. The model suggests how community statistics and time series of individual species can inform on the relative importance of the ecological processes that structure diversity.

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Ecol Lett. 2026 Feb ;29(2):e70333. doi : 10.1111/ele.70333.

In vivo autofluorescence lifetime imaging of spatial metabolic heterogeneities and learning-induced changes in the Drosophila mushroom body

Tommaso VILLA — 2026-02-12T08:52:21Z

Authors
Philémon Roussel, Mingyi Zhou, Chiara Stringari, Thomas Preat, Pierre-Yves Plaçais, Auguste Genovesio

Abstract

Neuronal energy regulation is increasingly recognized as a critical factor underlying brain functions and their pathological alterations, yet the metabolic dynamics that accompany cognitive processes remain poorly understood. As a label-free and minimally invasive technique, fluorescence lifetime imaging (FLIM) of coenzymes NADH and NADPH (collectively referred to as NAD(P)H) offers the possibility to resolve cellular metabolic profiles with high spatial precision. However, NAD(P)H FLIM's capacity to detect subtle variations in neuronal metabolism has not been demonstrated. In this study, we applied NAD(P)H FLIM to map the metabolic profiles of Drosophila neurons in vivo across multiple scales, focusing on the primary centers for associative memory : the mushroom bodies (MBs). At a broad scale, we obtained an overview of the metabolic signatures of the main brain tissue and identified a marked difference between neuropil and cortex areas. At a finer scale, our findings revealed notable heterogeneity in the basal metabolic profiles of distinct MB neuron subtypes. Measurements performed after associative olfactory learning also uncovered a low-magnitude subtype-specific metabolic shift associated with memory formation, suggesting the utility of NAD(P)H FLIM in detecting physiology-driven changes linked to brain function. These results establish a promising framework for studying the spatial heterogeneities and the dynamics of cerebral energy metabolism in vivo.

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Elife. 2026 Feb 9:14:RP106040. doi : 10.7554/eLife.106040.

mTOR controls ependymal cell differentiation by targeting the alternative cell cycle and centrosomal proteins

Tommaso VILLA — 2026-01-21T11:43:35Z

Authors
Alexia Bankolé, Ayush Srivastava, Asm Shihavuddin, Khaled Tighanimine, Marion Faucourt, Vonda Koka, Solene Weill, Ivan Nemazanyy, Alissa J Nelson, Matthew P Stokes, Nathalie Delgehyr, Auguste Genovesio, Alice Meunier, Stefano Fumagalli, Mario Pende, Nathalie Spassky

Abstract

Ependymal cells are multiciliated glial cells lining the ventricles of the mammalian brain. Their differentiation from progenitor cells involves cell enlargement and progresses through centriole amplification phases and ciliogenesis. These phases are accompanied by the sharp up-regulation of mTOR Complex 1 activity (mTORC1), a master regulator of macromolecule biosynthesis and cell growth, whose function in ependymal cell differentiation is unknown. We demonstrate that mTORC1 inhibition by rapamycin preserves the progenitor pool by reinforcing quiescence and preventing alternative cell cycle progression for centriole amplification. Overexpressing E2F4 and MCIDAS circumvents mTORC1-regulated processes, enabling centriole amplification despite rapamycin, and enhancing mTORC1 activity through positive feedback. Acute rapamycin treatment in multicentriolar cells during the late phases of differentiation causes centriole regrouping, indicating a direct role of mTORC1 in centriole dynamics. By phosphoproteomic and phosphomutant analysis, we reveal that the mTORC1-mediated phosphorylation of GAS2L1, a centrosomal protein that links actin and microtubule cytoskeletons, participates in centriole disengagement. This multilayered and sequential control of ependymal development by mTORC1, from the progenitor pool to centriolar function, has implications for pathophysiological conditions like aging and hydrocephalus-prone genetic diseases.

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EMBO Rep. 2025 Jun ;26(12):3075-3105. doi : 10.1038/s44319-025-00460-2.

Loss of macroevolutionary species fitness explains the rise and fall of clades

Tommaso VILLA — 2026-01-14T17:49:13Z

Abstract

How and why species diversity varies over geological timescales remains disputed. Debate revolves around the existence of equilibrium dynamics, the predominance of adaptive radiations and the relative importance of speciation and extinction in driving diversity trajectories. We analyse the evolutionary history of 27 radiations of plants, arthropods and vertebrates, with phylogenetic information incorporating extinct and extant species under a new 'fossilized birth-death diffusion' model that provides a detailed characterization of past diversification and resulting diversity dynamics. Here, lineages undergo speciation and extinction rates that diffuse continuously in time and generate fossils with rates that can vary with stratigraphy. Clade diversity trajectories follow rise and decline dynamics, with fast accumulation following recurrent speciation while slowdowns and losses are modulated primarily by changes in extinction. Diversity dynamics do not appear to be governed by clade-level processes expected from adaptive radiations or diversity dependence. Rather, these patterns emerge from dynamics at the species level, where lineages tend to become increasingly vulnerable to extinction and less likely to speciate with time. Those species that counteract this trend create and maintain biodiversity through deep time. The rise and fall of clades results from species-level fates.

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Nat Ecol Evol. 2025 Dec ;9(12):2346-2357. doi : 10.1038/s41559-025-02873-7.

A low-level Cdkn1c/p57kip2 expression in spinal progenitors drives the transition from proliferative to neurogenic modes of division

Tommaso VILLA — 2026-01-05T15:23:18Z

Authors
Baptiste Mida, Nathalie Lehmann, Rosette Goïame, Fanny Coulpier, Kamal Bouhali, Isabelle Barbosa, Hervé Le Hir, Morgane Thomas-Chollier, Evelyne Fischer^#, Xavier Morin^#

Abstract

During vertebrate neurogenesis, a transition from symmetric proliferative to asymmetric neurogenic divisions is critical to balance growth and differentiation. Using single-cell RNA-seq data from the chick embryonic neural tube, we identify the cell cycle regulator Cdkn1c as a key regulator of this transition. While Cdkn1 is classically associated with neuronal cell cycle exit, we show that its expression initiates at low levels in neurogenic progenitors. Functionally targeting the onset of this expression impacts the course of neurogenesis : Cdkn1c knockdown impairs neuron production by favoring proliferative symmetric divisions. Conversely, inducing a low-level Cdkn1c misexpression in self-expanding progenitors forces them to prematurely undergo neurogenic divisions. Cdkn1c exerts this effect primarily by inhibiting the CyclinD1-CDK4/6 complex and G1 phase lengthening. We propose that Cdkn1c acts as a dual driver of the neurogenic transition whose low level of expression first controls the progressive entry of progenitors into neurogenic modes of division before higher expression mediates cell cycle exit in daughter cells. This highlights that the precise control of neurogenesis regulators' expression sequentially imparts distinct functions essential for proper neural development.

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EMBO Rep. 2025 Dec 8. doi : 10.1038/s44319-025-00653-9.

Unequal mitochondrial segregation promotes asymmetric fates during neurogenesis

Tommaso VILLA — 2026-01-05T15:21:36Z

Abstract

Asymmetric cell division plays a critical role during vertebrate neurogenesis by generating neuronal cells while maintaining a pool of progenitors. It relies on unequal distribution of cell fate determinants during progenitor division. Here, we use live imaging in the chick embryonic neuroepithelium to demonstrate that mitochondria behave as asymmetric fate determinants during mitosis. We show that the frequency of unequal distribution of mitochondria increases in parallel with the rate of asymmetric divisions during development. Furthermore, fate tracking experiments reveals that following progenitor division, a cell inheriting fewer mitochondria than its sister consistently differentiates into a neuron. We set up a chemogenetic approach to experimentally displace mitochondria specifically during mitosis to force their unequal inheritance and find that this drives premature neuronal differentiation. In this work, we establish a direct causal relationship between unequal mitochondrial inheritance and the asymmetric fate of sister cells in vivo, revealing a pivotal mechanism for neurogenesis.

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Coverage of the article on the CNRS INSB website

Coverage of the article on the Le Monde website (under paywall)

Nat Commun. 2025 Dec 15 ;16(1):11049. doi : 10.1038/s41467-025-66932-0.