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La naissance de la tectonique globale
No full textInternational audienceIn this review, the birth of plate tectonics is described by Xavier Le Pichon through extensive work in marine geophysics. The seafloor spreading hypothesis proposed by Hess in 1959 marked a turning point as supported by the alternation of normal and inverse magnetization bands of the ocean floor discovered by Vine and Matthews in 1963. These symmetrical bands, caused by geomagnetic reversals, allow dating of the crust and measurement of spreading rates. The lack of sediment deformation indicates that these displacements take place as the motion of rigid blocks. Considering these motions as rotations around poles then accounts for mid-oceanic ridges, trenches, and transform faults. A six-plate model, bounded by seismic zones and ridges allow global seismicity to be explained. In this way global tectonics emerges to become the unifying framework of Earth sciences.Dans cet article, la genèse de la tectonique des plaques est retracée par Xavier Le Pichon à partir des travaux en géophysique marine. L'hypothèse du renouvellement des fonds océaniques proposée par Hess en 1959 marque un tournant décisif, étayée par les alternances de bandes d'aimantation normale et inverse de ces fonds découverte par Vine et Matthews en 1963. Dues aux inversions du champ magnétique, ces bandes d'aimantation symétriques permettent de dater la croûte et de mesurer sa vitesse d'expansion. L'absence de déformations dans les sédiments indique par ailleurs que cette croûte subit des déplacements sous forme de blocs rigides. Considérer ces déplacements comme des rotations autour de pôles rend alors compte des dorsales, des fosses océaniques et des failles transformantes. Un modèle à six plaques principales, délimitées par les dorsales et des zones fortement sismiques, s'accorde de la sorte avec la sismicité globale. Ainsi naît la tectonique globale pour devenir aujourd'hui le cadre unificateur des sciences de la Terre
Unlocking sugar subcellular dynamics: The crucial function and regulation of tonoplast sugar transporters in plant response to climate change
No full textInternational audienceAbstract Tonoplast sugar transporters are key regulators of intracellular sugar partitioning, mediating sugar flux between the cytosol and vacuole—an essential process for plant development and stress adaptation. Recent advances have deepened our understanding of well-characterized transporters such as TSTs and SWEETs, while also expanding the transporter repertoire with newly identified members including SWEET2, ERDL4, and SFP1/SAST1 across diverse plant species, including crops. Despite these insights, the regulatory mechanisms controlling transporter activity remain largely unresolved. This review aims to consolidate this expanding body of knowledge and explore in greater depth the molecular regulatory mechanisms controlling tonoplast sugar transporters. Additionally, we also analyze publicly available expression datasets to evaluate the potential of these transporters as targets for improving plant resilience under climate change conditions, particularly in response to elevated atmospheric CO₂. Ultimately, this review presents a new perspective on the significance of studying tonoplast sugar transporters, aiming to develop innovative strategies that enhance plant resilience to environmental challenges
Vecchio, un greco non può esserlo
No full textTraduction italienne de Vieux un Grec ne peut pas l''être, Paris, Belles Lettres, 2023International audienc
A transient mutational burst occurs during yeast colony development
No full textInternational audienceCharacterizing the contribution of mutators to mutation accumulation is essential for understanding cellular adaptation and diseases like cancer. By measuring single and double mutation rates, including point mutations, segmental duplications, and reciprocal translocations, we found that wild-type yeast colonies exhibit double mutation rates up to 17 times higher than expected from experimentally determined single mutation rates. These double mutants retained wild-type mutation rates, indicating they originated from genetically normal cells that transiently expressed a mutator phenotype. Numerical simulations suggest that transient mutator subpopulations likely consist of less than a few thousand cells, and experience high-intensity mutational bursts for less than five generations. Most double mutations accumulated sequentially across cell cycles, with simultaneous acquisition being rare and likely linked to systemic genomic instability. Additionally, we explored the genetic control of transient hypermutation and found that the excess of double mutants can be modulated by replication stress and the DNA damage tolerance pathway. Our findings suggest that transient mutators play a significant role in genomic instability and contribute to the mutational load accumulating in growing isogenic populations
Abnormal Connectivity of the Head Neural Integrator in Cervical Dystonia
No full textInternational audienceBackgroundCervical dystonia is characterized by abnormal neck and head movements, possibly related to a dysfunction of the interstitial nucleus of Cajal (INC) and the head neural integrator, a system responsible for the control of head and eye movements. However, neuroanatomical evidence of alterations in the head neural integrator in cervical dystonia is sparse.ObjectivesWe investigated structural and functional integrity of the INC and its connections in cervical dystonia.MethodsThis cross-sectional, observational study compared 19 cervical dystonia patients and 21 healthy controls, using anatomical, diffusion-weighted, and resting-state functional images. We reconstructed tracts converging on the INC, and involved in the control of head movements. We evaluated group differences in microstructural integrity using fixel-based analysis, and effective connectivity using dynamic causal modeling.ResultsCompared with controls, patients showed microstructural abnormalities within the INC and cerebral peduncle. Effective connectivity showed abnormal self-inhibition in the INC, substantia nigra, and vermis in patients, with decreased excitation from the substantia nigra to the INC, increased inhibition from the deep cerebellar nuclei and primary sensorimotor cortex, and decreased excitation from the INC to the cerebellar vermis.ConclusionsA dysfunction of the INC might contribute to altered sensorimotor integration in cervical dystonia, and abnormal feedback from its afferent connections could alter its integrative function, resulting in a disturbed head and neck posture. © 2025 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society
Deferasirox derivatives as inhibitors of Kallikrein‐related peptidases associated to neurodegenerative diseases
No full textInternational audienceKallikrein‐related peptidases are a family of serine proteases which loss of activity regulation has been particularly linked to neurodegenerative diseases. Moreover, iron overload is also a key process in some of these leading pathological conditions, particularly Alzheimer’s disease. We identified for the first time Deferasirox, a well‐known FDA‐approved iron chelator (DFX) as an initial hit for kallikrein’s (KLK) inhibition and propose here the design and synthesis of a small library of molecules using DFX as chemical scaffold. Resulting sub‐series of compounds were evaluated against lead central nervous system KLK’s, namely KLK1, KLK6 and KLK8 using targeted pharmacomodulations on DFX. Beyond DFX, several reversible micromolar inhibitors of these KLKs have been identified as hits and were shown to be devoid of any noticeable cytotoxicity towards neural cell lines commonly used in the field of neurodegenerative diseases. Their ability to chelate iron was also assessed in comparison to DFX and preformed iron‐compound complexes displayed slightly improved inhibition potency for some derivatives with a KLK‐dependent manner. Hence, we identified several DFX derivatives as promising starting points for the development of dual therapeutic agents in the context of neurodegenerative diseases where both deregulated KLK’s proteolysis and iron dysregulation are involved
La signalisation calcique nucléaire dans les neurones exprimant le récepteur D1 du noyau accumbens régule les adaptations moléculaires, cellulaires et comportementales à la cocaïne
No full textInternational audienceBACKGROUND: The persistence of cocaine-evoked adaptations relies on gene regulations within the reward circuit, especially in the ventral striatum (i.e., nucleus accumbens [NAc]). Notably, activation of the ERK (extracellular signalregulated kinase) pathway in the striatum is known to trigger a transcriptional program shaping long-term responses to cocaine. Nuclear calcium signaling has also been shown to control multiple forms of transcription-dependent neuroadaptations, but the dynamics and roles of striatal nuclear calcium signaling in preclinical models of addiction remain unknown. METHODS: A genetically encoded cell type-specific nuclear calcium probe has been developed to monitor calcium dynamics in the nuclei of striatal neurons, including in freely moving mice. A cell type-specific inhibitor of nuclear calcium signaling combined with 3-dimensional imaging of neuronal morphology, immunostaining, and behavior was used to disentangle the roles of nuclear calcium in NAc medium spiny neurons (MSNs) expressing the dopamine D 1 receptor (D1R) or D 2 receptor (D2R) on cocaine-evoked responses. RESULTS: The D1R-mediated potentiation of calcium influx through glutamate NMDA receptors, which shapes cocaine effects, also drives nuclear calcium transients. Fiber photometry revealed that cocaine-treated mice showed a sustained nuclear calcium increase in NAc D1R-MSNs. Disrupting nuclear calcium in D1R-MSNs, but not D2R-MSNs, blocked cocaine-evoked morphological changes of MSNs and gene expression and blunted cocaine's rewarding effects. CONCLUSIONS: Our study unravels the dynamics and roles of cocaine-induced nuclear calcium signaling increases in D1R-MSNs on molecular, cellular, and behavioral adaptations to cocaine and represents a significant breakthrough because it could contribute to the development of innovative strategies with therapeutic potential to alleviate addiction symptoms
