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Lundi 29 Avril 2024    11:00
Invite par: Hugues Aschard The department of Computational Biology will be organizing new Methods Primer seminar series addressing advanced analytical methods. The meetings will be in-person only using a chalk talk format. It aims at being an open ... Plus d'infos...
Tags: Molecular biology, Bioinformatics, DNA replication, Polymerase chain reaction, Primer, Computational biology
Annonce publiée le 11-04-2024
Institut Pasteur
Batiment Yersin, salle Yersin Building ground floor meeting room (24-RDC-02),
Lundi 29 Avril 2024    11:00
Invite par: IBENS Neuroscience Seminar When forced to choose between fundamental needs, making the wrong decision could prove fatal. However, it is currently unclear how alternative options are evaluated and appropriate actions are prioritised. To tackle this problem, we developed an experimental system to study the neural circuit mechanisms that integrate the benefit of imminent courtship success with the risk of predation in Drosophila. By combining our novel behavioural assay with neurogenetics, connectomics and live imaging, we identified the neural circuitry that establishes behavioural priority during this ?life-death' conflict. Crucially, we found that the probability of mating success defines the decision to reproduce or flee. Our work reveals how the brain weighs up antagonistic advantages and risks, and the probability of success, at a cellular-circuit level. Plus d'infos...
Tags: Mating, Courtship display, Connectomics, Neurogenetics, Human mating strategies, Perception
Annonce publiée le 23-04-2024
IBENS
salle Favard, IBENS 46 rue d'Ulm 75005 Paris
Lundi 29 Avril 2024    12:00
Neuronal differentiation requires building a complex intracellular architecture, and therefore the coordinated regulation of defined sets of genes. RNA-binding proteins (RBPs) play a key role in this regulation. However, while their action on individual mRNAs has been explored in depth, the mechanisms used to coordinate expression of the gene programs shaping neuronal morphology are poorly understood. To address this, we analysed how the RBP IMP1 (IGF2BP1), an essential developmental factor, selects and regulates its RNA targets during the differentiation of human neurons. We performed a combination of system-wide and molecular analyses, revealing that IMP1 developmentally transitions to and directly regulates the expression of mRNAs encoding essential regulators of the microtubule network, a key component of neuronal morphology. Furthermore, we showed that m6A methylation drives the selection of specific IMP1 mRNA targets and their protein expression during the developmental transition from neural precursors to neurons, providing a molecular principle for the onset of target selectivity. Plus d'infos...
Artificial Intelligence is a broad term that is often misunderstood. Its subfields, such as machine and deep learning have achieved astonishing performances, such as some Large Language Models passing the Turing Test or AlphaFold offering a solution to a 50 years old problem. Because new technologies in medecine and biology generate massive amounts of high quality data (omics, images, clinicals, molecules …), there is an opportunity to leverage machine learning tools to extract relevent information and find new discoveries from these datasets. In this presentation, we will demystify machine learning to give you intuition on how it works and how it could be applied to your project. We will also cover specific deep learning applications in biology and present its future possibilities and limits through foundational models.
How randomly injured animals can appropriately re-establish positional information and control the deployment of repair programs are key questions of regenerative biology. The hydrozoan jellyfish Clytia hemisphaerica has recently emerged as an original model organism for probing repair phenomena, thanks to its remarkable regenerative abilities. Coping with frequent injuries in the planktonic environment, Clytia efficiently restores its circular morphology within 12 hours and regenerates missing structures, such as the mouth, in 4 days. Our investigations uncovered a complex interplay of mechanical forces, cellular migration, and proliferation, underlying this rapid recovery process. During umbrella reshaping, the distinct configurations of the rearranging radial muscle fibres – which can be likened to topological defects - correlate with differential patterns of Wnt signalling activation; they function as positional cues, regulating the fate of the wound and the initiation of organ regenerative programs. Regenerative morphogenesis involves a combination of localized cell proliferation and long-range cell recruitment. Leveraging the unique regenerative process of Clytia, and the recent technological developments of the model, we have started unravelling the mechanical and transcriptional interplay in repairing tissues - combining omics, live imaging, modelling and functional approaches. Our findings not only offer insights into the universal principles governing patterning formation and morphogenesis in physiologically complex adult organisms, but also shed light on the evolutionary trajectories of regenerative capacities and stem cells within metazoans.
Tags: Jellyfish, Regeneration, Common Threads, Thread
Annonce publiée le 18-04-2024
Institut Curie
Centre de recherche - Paris - Amphitheatre Helene Martel-Massignac (BDD)
Jeudi 02 Mai 2024    11:30
Claude Desplan1,2, Nikos Konstantinides1, Felix Simon1, Neset Ozel1, Isabel Holguera1, Jennifer Malin1, Yen Chen1, and Bogdan Sieriebriennikov1
1 Center for Developmental Genetics, Department of Biology, New York University, New York, USA; 2 Center for Genomics and System Biology, NYU Abu Dhabi, UAE.
In the Drosophila optic lobes, ~250 neuronal types organized as 800 columns process the inputs from 800 unit-eyes. Neural stem cells in the medulla sequentially express a series of temporal transcription factors (tTFs), producing at each temporal window different neurons that innervate each of the 800 columns. We used single-cell mRNA sequencing to identify the tTFs that specify most medulla neurons. Each tTF regulates the progression of the series by activating the next tTF and repressing the previous one. Furthermore, the neuroepithelium that generates these stem cells is patterned into subdomains by spatial TFs: Although the series of tTFs is the same in stem cells originating from all spatial domains, the neurons they produce differ. Therefore, the integration of temporal and spatial patterning as well as Notch status, are sufficient to explain the generation of the entire neuronal diversity in this brain region.
Finally, we will show how diversity in the brain can evolve to affect specific sensory functions in different species. I will describe the dramatically increased diversity in the mushroom body in ants as compared to flies, as ants rely extensively on pheromones rather than vision for their eusocial life.
Centre de recherche - Orsay - Amphitheatre du Batiment 111
Jeudi 02 Mai 2024    13:30
Training objectives
- Understand the legal definitions of sexist and sexual violence - Understand the main figures on the subject - Understand the consequences of gender-based and sexual violence - Understand the employer's responsibilities and obligations, as well as sanctions and procedures. - Know how to listen and provide guidance
Tags: Criminology, Violence against men, Violence against women, Sex crimes, Crimes against women, Sexual violence, Initiatives to prevent sexual violence, Causes of sexual violence
Annonce publiée le 06-02-2024
Institut Curie
Centre de recherche - Paris - Webinar
Vendredi 03 Mai 2024    11:00
Aging is associated with a decline in tissue function and the onset of a constellation of diseases. We are interested in understanding aging, with a particular focus on brain aging. Because aging is complex, we use organisms with diverse lifespans – the worm C. elegans, the African killifish, the mouse, and cells from mice and humans. We are interested in identifying epigenetic and metabolic pathways involved in delaying aging in response to external stimuli, including nutrients and the opposite sex. Our lab is also interested in using mouse models to address complex questions about mammalian aging, notably the regulation of regenerative neural stem cells and their progeny during aging. Finally, we are pioneering the naturally short-lived African killifish as a new model to identify principles underlying vertebrate aging and “suspended animation”. We hope that these discoveries will identify new strategies to delay, suspend, or even reverse aspects of aging and age-related diseases.
Nos recherches visent à élucider comment la croissance et la division cellulaires sont régulées dans l'espace et dans le temps, notamment par la dégradation sélective des composants cellulaires. Les cellules eucaryotes utilisent l'autophagie et le système ubiquitine-protéasome (UPS) pour assurer l'homéostasie cellulaire et recycler les composants excédentaires et non essentiels en réponse à la privation de nutriments. Pourtant, des mécanismes doivent exister pour protéger les composants cellulaires essentiels afin de reprendre la croissance cellulaire après la libération du stress. Cependant, malgré leur importance fondamentale pour la santé et la maladie, on sait peu de choses sur la manière dont ces processus antagonistes sont régulés et coordonnés dans les cellules affamées et dormantes. Pour répondre à ces questions fondamentales, nous utilisons des cellules de levure et de mammifères pour étudier comment les cellules protègent les composants cellulaires essentiels tels que les ribosomes et les enzymes métaboliques clés. En utilisant la pyruvate kinase (PK) Cdc19 de levure comme paradigme, nous avons récemment découvert que cette enzyme forme des fibres réversibles qui ressemblent à des structures de type amyloïde. Les amyloïdes ont longtemps été considérées comme des agrégats pathologiques irréversibles, souvent associés à des maladies neurodégénératives. Cependant, des découvertes récentes remettent en question ce point de vue, en fournissant la preuve que des amyloïdes réversibles se forment dans des conditions de stress et remplissent des fonctions cellulaires cruciales. Pourtant, les mécanismes moléculaires régulant les amyloïdes fonctionnels et les différences avec leurs homologues pathologiques restent mal compris. Nous démontrons que la levure et la PK humaine (PKM2) forment des agrégats réversibles via un noyau amyloïde sensible au pH. L'acidification cytosolique induite par le stress favorise la formation d'agrégats via la protonation de résidus spécifiques de glutamate ou d'histidine au sein du motif du noyau amyloïde. Les mutations imitant la protonation entraînent une agrégation constitutive de la PK, tandis qu'à l'inverse, un mutant PK non protonable reste soluble même dans des conditions de stress. L'agrégation physiologique de la pharmacocinétique est couplée au recâblage métabolique et à l'arrêt de la glycolyse, et une mauvaise régulation de ce processus entraîne de graves défauts de croissance. Nos travaux révèlent ainsi un mécanisme moléculaire conservé au cours de l’évolution et potentiellement répandu qui régit la fonctionnalité et la réversibilité amyloïde, déclenché par un changement de pH physiologique lors d’un stress.
Centre de recherche - Paris - Amphitheatre Constant-Burg - 12 rue Lhomond, Paris 5e
Lundi 13 Mai 2024    11:00
The Roose team at UCSF studies mechanisms of cell-cell interactions in immunology and cancer1-7, with emphasis on personalized medicine4,8 and single cell approaches9-11. Over the past 7 years, we shifted a large portion of our research efforts to understanding human biology and disease. We are deeply interested in the cellular networks that underpin autoimmune diseases and cancer, which I will talk about in my seminar at the Curie Institute. We “deconstruct” these diseases with single cell technology to generate hypotheses on disease-driving cellular networks.
Through our work on cancer & stem cells, we optimized organoid protocols, propagating, characterizing, and biobanking patient organoids. In my seminar I will cover the organoid pipelines we established in my lab and will present how we are combining these organoids with epithelial cell types together with other patient cell types in assembloids. I will particularly focus on how we are using assembloids to “reconstruct” disease and better understand cancer-immune cell crosstalk. We aim to deconstruct and reconstruct T cell subsets and explore functional T cell programs in the context of cancer metastasis and cancers for which immunotherapy needs to be improved. We believe that assembloids offer many opportunities to make basic research discoveries with direct translational potential.
Hopital site de Paris - Amphitheatre Helene Martel-Massignac (BDD)
Mardi 14 Mai 2024    9:30
The functioning of genome-wide gene regulatory networks in bacteria presents us with an apparent paradox. On the one hand, bacterial populations successfully coordinate their gene expression patterns and phenotypes to allow them to grow in a huge variety of environments, including complex combinations of nutrients and stresses that natural selection cannot possibly have specifically prepared them for. For example, bacteria can even adapt their phenotype to grow in fully deuterated water. On the other hand, the more we study gene regulation in bacteria at the single cell level, the more noisy and haphazard it appears. Moreover, given the low molecule numbers involved, there are severe thermodynamic limitations on the accuracy of both sensing and regulation of gene expression in single bacterial cells, which seem to preclude the robust adaptation that is observed at the population level. In this talk, I will present a new picture that is emerging from recent joint experimental and theoretical studies of gene regulation at the single-cell level in bacteria, suggesting a subtle stochastic strategy for phenotypic adaptation in which noise and regulation are deeply entangled. The key experimental observations that form the main ingredients of this picture include:
1. That gene expression fluctuations are largely driven by propagation of noise through the gene regulatory network, 2. That, through the effects of dilution, growth rate controls the sensitivity of gene regulatory circuits to fluctuations, and 3. That gene expression noise and phenotypic fluctuations systematically decrease with growth rate.
I will discuss how these observations combine into a stochastic strategy by which bacterial populations successfully adapt their phenotypes to complex unpredictable environments, in spite of highly noisy and inaccurate regulation at the single cell level.
Tags: Wolfram, Holy Grail, Middle High German literature, Conrad Wolfram, Catherine Wolfram
Annonce publiée le 08-11-2023
Laboratoire Jean Perrin
salle de seminaires 5eme etage - LJP - Tours 32-33
Mardi 21 Mai 2024    11:00
Invite par: Cassandra Koh Keywords: drug abuse, neurodevelopment, extracellular vesicles, basic science Plus d'infos...
Annonce publiée le 29-12-2023
Institut Pasteur
Batiment Jacob, salle Auditorium Francois Jacob,
Mardi 21 Mai 2024    11:00
DNA methylation is a broadly observed epigenetic modification. As genomic DNA methylation profiles dynamically change during development and aging, alterations in DNA methylation patterns are linked to diseases such as cancers and immunodeficiency. ICF syndrome is characterized by hypomethylation at heterochromatin. Of four proteins whose mutation cause ICF syndromes (DNMT3B, ZBTB24, CDCA7 and HELLS), we have previously demonstrated that CDCA7 is a critical activator for the nucleosome remodeling activity of the SNF2-family ATPase HELLS. As DNA methyltransferases cannot directly methylate DNA on the nucleosome, we suggested that the CDCA7-HELLS complex assists DNA methyltransferases by sliding DNA on the nucleosome. However, it remained unclear why the CDCA7-HELLS complex, among several SNF2-family proteins that can remodel nucleosomes, plays a unique role in DNA methylation. Here, I will share our efforts to fill this gap by showing that CDCA7 is an adaptor for hemimethylated CpG. Implications of this finding for diseases will be discussed.
Centre de recherche - Paris - Amphitheatre Constant-Burg - 12 rue Lhomond, Paris 5e
Mardi 21 Mai 2024    14:00
La taille des cellules joue un rôle crucial dans le fonctionnement de divers types de cellules dans tout le corps humain, influençant la structure des organites, la biosynthèse et les processus de transport en surface. Bien que certains gènes influençant la taille des cellules aient été identifiés, les mécanismes moléculaires par lesquels la croissance cellulaire initie la division cellulaire restent largement inconnus. Contrairement aux attentes selon lesquelles la croissance renforcerait l’activité des kinases dépendantes des cyclines (Cdks), connues pour faciliter la division cellulaire, nos résultats suggèrent le contraire. À savoir, cette croissance cellulaire provoque la division en diluant les protéines qui inhibent la division, en particulier Whi5 dans la levure et le suppresseur de tumeur du rétinoblastome (Rb) dans les cellules humaines. Cela a identifié la « dilution des inhibiteurs » comme un mécanisme critique reliant la croissance cellulaire à la division cellulaire. Nous rapportons ici nos nouvelles découvertes sur les mécanismes moléculaires distincts responsables de la diminution des concentrations de Rb et de Whi5 en phase G1. Nos résultats soulignent les stratégies moléculaires complexes utilisées par les cellules eucaryotes pour mettre en œuvre la stratégie conservée consistant à diluer les inhibiteurs du cycle cellulaire pendant la phase G1 afin de coordonner la croissance cellulaire avec la division.
Centre de recherche - Paris - Amphitheatre Constant-Burg - 12 rue Lhomond, Paris 5e
Mercredi 22 Mai 2024    0:00
Les participants auront l'occasion :
Le cours « NON-CODING GENOME » explorera la diversité des éléments d'ADN non géniques et des ARN non codants dans un large spectre de processus cellulaires, chez l'homme et les organismes modèles, ainsi que leur implication dans la physiologie et la pathologie. Des experts de renommée internationale présenteront leurs dernières découvertes relatives à l'identification et à la caractérisation fonctionnelle du génome non codant et discuteront de nouveaux concepts en matière de régulation et d'évolution du génome, en mettant l'accent sur les outils expérimentaux et informatiques. Les sessions thématiques incluront des ARN non codants longs et petits, des éléments transposables, des répétitions d'ADN structurel et des éléments régulateurs non codants. Ce cours offrira aux jeunes étudiants et aux chercheurs l’occasion d’élargir leurs connaissances et de discuter de leurs travaux avec une communauté scientifique internationale dans un environnement stimulant de l’Institut Curie à Paris.
Tags: Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society, Cell and molecular biology
Annonce publiée le 29-02-2024
Institut Cochin
Salle Rosalind Franklin
Jeudi 23 Mai 2024    11:00
Invite par: Emmanuelle FABRE Cells can rapidly and reversibly adopt distinct states and this can occur independently of genetic alterations, a biological mechanism commonly referred to as cell plasticity. CD44 is a plasma membrane glycoprotein associated with development, immune cell activation as well as tumorigenesis. Although often described as a cell-surface marker, the biological function of CD44 remains elusive. We discovered that CD44 mediates the uptake of metals including copper and iron bound to hyaluronates in cells from distinct tissues. This glycan-mediated metal endocytosis mechanism is enhanced during immune cell activation and in cancer cells undergoing epithelialmesenchymal transition. We found that copper(II) catalyzes a previously uncharted chemical reaction in mitochondria required for the production of key metabolites. In contrast, iron is required in the nucleus to promote the activity of specific demethylases. Together, these metals orchestrate metabolic and epigenetic programming of cell plasticity, establishing CD44 as a regulator of cell state transition. We developed new classes of small molecules that selectively interfere with these metal-catalyzed chemical processes in cells. Supformin specifically targets mitochondrial copper(II), thereby antagonizing macrophage activation in several pre-clinical models of acute inflammation and cancer. This validates a key concept in biology whereby pharmacological control of cell plasticity confers therapeutic benefits. This also suggest a competition for metal uptake by immune and cancer cells that may enable tumor progression. Structurally distinct classes of small molecule were developed to manipulate lysosomal iron providing control of cell fate with induction of or protection against ferroptosis . These findings illuminate a universal metal uptake mechanism and the critical role of metals as master regulators of cell plasticity, paving the way towards the development of next generation therapeutics. Plus d'infos...
Annonce publiée le 05-04-2024
UMR7212-U944
Batiment Jean Bernard
INSERM U944 UMR7212
IRSL
Hopital St Louis
16 rue de la Grange aux Belles
75010 PARIS
Vendredi 24 Mai 2024    9:30
Invite par: Hugues de The - College de France Plus d'infos...
Tags: @CirbCdf
Annonce publiée le 18-04-2024
College de France
Amphitheatre Halbwachs, 11 place Marcelin-Berthelot, 75005 Paris
Lundi 27 Mai 2024    9:00
Invite par: Cyril Renassia Annual symposium of the Labex IBEID A day dedicated to the scientific work of the Labex IBEID partners. This year we will have the pleasure to welcome Prof Bernhard Hube from Lebniz-Hans Knoll Institute. ... Plus d'infos...
Tags: Hube, LabEx ReFi - European Laboratory on Financial Regulation, French National Centre for Scientific Research
Annonce publiée le 04-04-2024
Institut Pasteur
Batiment: Duclaux Salle: Amphitheatre Duclaux
Jeudi 30 Mai 2024    0:00
The small interfering RNA pathway constitutes a pivotal antiviral defense against RNA viruses in insects, functioning through RNA interference mediated by Ago2-guided cleavage of viral genomes. This systemic mechanism requires the recognition and transport of double-stranded RNA (dsRNA) of viral origin. Despite the known cellular uptake of dsRNA through endocytosis, the specific protein(s) responsible for this internalization remain elusive. Here, we investigate the role of Hsc70-4, a cytosolic protein known for its chaperone activity, as a potential cell surface receptor or co-receptor for dsRNA internalization in the insect model Drosophila melanogaster. Immunofluorescence assays were conducted on permeabilized and non-permeabilized S2 cells using a specific anti-Hsc70-4 antibody to determine its subcellular localization. Permeabilized cells exhibited cytoplasmic and plasma membrane staining, whereas non-permeabilized cells showed punctate staining on the outer surface of the plasma membrane, indicating the presence of Hsc70-4 in the cell surface. To assess the role of Hsc70-4 as a receptor/co-receptor for dsRNA uptake, we employed immunofluorescence and luciferase-based silencing assays. Pretreatment of S2 cells with anti-Hsc70-4 antibody significantly reduced the internalization of Cy3-labeled dsRNA, suggesting Hsc70-4's involvement in the uptake process. Luciferase assays revealed a direct correlation between antibody concentration during pretreatment and decreased silencing efficiency, further supporting Hsc70-4's role as a dsRNA receptor. Finally, we evaluated the ability of Hsc70-4’s to bind dsRNA in vitro using electrophoretic mobility shift assays and found that Hsc70-4 binds specifically dsRNA in a sequence independent manner. Altogether, our experiments provide evidence that Hsc70-4 is expressed on the cell surface of drosophila cells where it may act as a receptor for extracellular dsRNA. These finding constitutes a previously undescribed function for Hsc70-4, and sheds light on the molecular mechanisms underlying insect antiviral defense. Invited by Suzanne Faure-Dupuy, Alberto De la Iglesia and Hugo Barreto, as part of the Post-doc seminar series. Plus d'infos...
V(D)J recombination is essential for generating the adaptive immune response and unlimited number of different antibodies and antigen receptors. Encoded by multiple V, D and J gene segments, antigen receptors are assembled by programmed double-stranded DNA cleavage and imprecise re-joining. RAG1/2 recombinase initiates the process by stochastically cleaving DNA at a pair of recombination signal sequences (RSS) bordering the V, D or J gene segments. DNA double strand cleavage occurs in a single active site in two consecutive steps, hydrolysis and strand transfer, resulting in DNA hairpin on the coding end and DSB on the RSS side. Coding ends processing and joining to complete V, D, and J gene assembly and circularization of RSS end are carried out by the non-homologous end joining process (NHEJ). The DNA-dependent protein kinase (DNA-PK), consisting of the catalytic subunit (DNA-PKcs) and Ku70/80, is the key player in NJEJ by protecting broken DNA ends, promoting DNA hairpin end opening and also coordinating nucleotide removal, addition and DNA end ligation. In this seminar I will report the molecular mechanism of DNA cleavage by RAG1/2 and regulation of NHEJ by autophosphorylation of DNA-PKcs.
Centre de recherche - Paris - Amphitheatre Marie Curie
Vendredi 31 Mai 2024
Invited by the Ladoux/Mege Lab, Christophe Leterrier (Aix Marseille Universite?, CNRS, INP, NeuroCyto Lab) will present an IJM seminars on the theme: The axonal cytoskeleton down to the nanoscale Abstract: The intricate arborization and molecular identity of axons is maintained for decades, but must also continuously adapt to changes in the environment and modulate the activity of neurons. Axons fulfill these paradoxical demands thanks to a unique cytoskeletal organization that ensures the coordinated transport, anchoring and assembly of axonal components. In our lab, we use super-resolution microscopy to delineate and map the nanoscale architecture of cytoskeletal structures within the axon: the periodic actin/spectrin submembrane scaffold, intra-axonal hotspots and trails, presynaptic actin assemblies, clathrin-coated pits. We are exploring their molecular organization and functions by combining versatile labeling approaches, correlative live-cell/super-resolution/electron microscopy and quantitative analysis that allow for high-content, nanoscale interrogation of the axonal architecture. The seminar will take place on Friday, May Plus d'infos...
The transcriptional activities of developmental genes in time, in space, or in defined cell-types are orchestrated by repertoires of enhancers that communicate in the 3D nuclear space with target promoters. Transcriptional outcomes, necessary to instruct morphogenesis, also involve defined transcriptional durations over which a gene product exerts its function. This aspect implies that genes’ transcriptional activities are initiated in different cells and trans-environment than the one where they are maintained later on or eventually repressed. Despite this intuitive concept, little is known about the cis-regulatory components that enable it. Here, we have established the regulatory trajectory framework to track how regulatory landscapes control gene transcription in vivo over long developmental time periods. Gene regulatory trajectories first involve transcriptional initiation, which corresponds to the onset of gene expression, followed by maintenance over time, and finally decommissioning, leading to gene repression. Using fluorescent sensors and recorders, we can sort cell populations from embryos at different phases of regulatory trajectories to characterize transcription, chromatin states, and genome topologies. Furthermore, we can engineer complex alleles to assess the role of cis-regulatory regions in controlling the phases of a gene’s regulatory trajectory. In summary, our approach aims to characterize the lifespans of developmental gene regulation and their functional dependencies. Guillaume Andrey is invited by Antoine Zalc. Plus d'infos...
Each limb muscle is unique with a specific shape, size and insertions to bone via connective tissues, so the developmental programs of muscle and associated connective tissues have to be tightly regulated to achieve the final muscle pattern. Although each limb muscle is unique, every muscle displays the same organization, they are all attached to tendons at both extremities and innervated at the center of muscle, defining the muscle domains. We found that muscle fusion is not homogenous within muscle but organized according to these domains. We also identified an unexpected recruitment of fibroblast nuclei in muscle fibers, recruitment localized at muscle tips, close to tendon. The spatial regulation of myogenesis is important to shape limb muscles during development. Delphine Duprez is invited by Pascal Maire. Plus d'infos...
Invite par: Cassandra Koh Keywords: Genome instability, DNA replication, replication stress, centromere, DNA damage Plus d'infos...
Tags: DNA replication, Chromosomes, Molecular genetics, Cell cycle, DNA replication stress, Centromere, Genome instability, S phase, DNA
Annonce publiée le 29-12-2023
Institut Pasteur
Batiment JACOB , salle Auditorium Francois JACOB ,
Jeudi 27 Juin 2024    0:00
Aging is associated with the accumulation of senescent cells and the increase of systemic inflammation. At the cellular level, aneuploidy gradually increases with age, suggesting that centromeric function may be dysregulated during aging, thereby contributing to senescence and inflammaging. Here, we investigated the regulation of centromere integrity in T lymphocytes, which exhibit age-associated aneuploidy and senescent cell accumulation. We have found that resting human lymphocytes from adults harbor a significant population of cells expressing low levels of total CENP-A, while CENP-B and CENP-C levels are not affected. Notably, CENP-A-low cells show lower or non-detectable CENP-A loaded at centromeres, indicating a change in centromere identity. In contrast, T cells from newborns do not exhibit this population. Furthermore, CENP-A-low T cells are not equally distributed among subsets of adult T cells. This indicates that the CENP-A-low state is associated with age-dependent changes and the functional state of T cells. In vitro, activated T cells in which we have recapitulated this defective centromere structure by genetic knock-out of CENP-A, show a senescent phenotype characterized by the upregulation of p53 target genes and the expression of proinflammatory genes. In addition, CENP-A knock-out T cells display chromosome-specific aneuploidy after proliferation. Overall, our results reveal that centromere structure integrity is impacted through lifespan and determines aneuploidy in T cells, contributing to regulation of senescence and inflammation. Invited by Suzanne Faure-Dupuy, Alberto De la Iglesia and Hugo Barreto, as part of the Post-doc seminar series. Plus d'infos...
Tags: Cell biology, Senescence, Chromosomal abnormalities, Cytogenetics, Cells, Cellular senescence, Centromere, Inflammaging, Aneuploidy, T cell, Kinetochore, Tim J. Yen
Annonce publiée le 16-12-2023
Institut Cochin
Salle Rosalind Franklin
Jeudi 04 Juillet 2024    0:00
Facioscapulohumeral muscular dystrophy (FSHD) is a complex neuromuscular disorder characterized by progressive weakness and atrophy of specific groups of muscles. Despite significant advancements in research, elucidating the precise pathophysiological mechanisms underlying FSHD remains a challenging endeavor. To tackle this challenge, we developed an integrated and interdisciplinary approach starting from genotype identification to tissue bioengineering to unravel the intricacies of FSHD pathophysiology.
Leveraging advancements in genomic technologies, we uncovered novel genetic variants and modifiers implicated in FSHD, expanding our understanding beyond the canonical genetic defect.
To complement genotype-based studies, we recently developed tissue bioengineering approaches to recapitulate the FSHD phenotype in vitro.
By considering the diversity of patient’s genotype, this interdisciplinary approach offers a comprehensive framework for dissecting FSHD pathophysiology from a molecular to a cellular level for the identification of the molecular cascades driving disease progression toward the development of treatment strategies. Frédérique Magdinier is invited by Pascal Maire. Plus d'infos...
Early human development remains mysterious and difficult to study. Recent advances in developmental biology, stem cell biology and bioengineering have contributed to a significant interest in constructing controllable, stem cell-based models of human embryo and organs (embryoids / organoids). The controllability and reproducibility of these human development models, coupled with the ease of genetically modifying stem cell lines, the ability to manipulate culture conditions and the simplicity of live imaging, make them robust and attractive systems to disentangle cellular behaviors and signaling interactions that drive human development. In this talk, I will describe our effort in using human pluripotent stem cells (hPSCs) and bioengineering tools to develop controllable models of the peri-implantation embryonic development and early neural development. The peri-implantation human embryoids recapitulate early post-implantation developmental landmarks, including amniotic cavity formation, amniotic ectoderm-epiblast patterning, primordial germ cell specification, development and organization of embryonic germ layers, yolk sac formation, and primitive hematopoiesis. I will further discuss an hPSC-based, microfluidic neural tube-like structure (or µNTLS), whose development recapitulates some critical aspects of neural patterning in both brain and spinal cord regions and along both rostrocaudal and dorsoventral axes. The µNTLS is further utilized for studying development of different neuronal lineages, revealing pre-patterning of axial identities of neural crest progenitors and a role of neuromesodermal progenitors in spinal cord and trunk neural crest development. We have further developed dorsoventral patterned, microfluidic forebrain-like structures (µFBLS) with spatially segregated dorsal and ventral regions and layered apicobasal cellular organizations that mimic human embryonic brain development in pallium and subpallium areas, respectively. Together, both µNTLS and µFBLS offer 3D lumenal tissue architectures with an in vivo-like spatiotemporal cell differentiation and organization, useful for studying human neurodevelopment and disease.
Tags: Embryology, Human embryonic development, Embryo donation, Ectogenesis
Annonce publiée le 22-04-2024
Institut Curie
Centre de recherche - Paris - Amphitheatre Marie Curie
Jeudi 12 Septembre 2024    0:00
Nicolas Reynoird is invited by Frédéric Pendino. Plus d'infos...
Tags: Dauphin, Grenoble
Annonce publiée le 19-03-2024
Institut Cochin
Salle Rosalind Franklin
Jeudi 12 Septembre 2024    13:30
Objectifs pédagogiques de la formation
- Connaître les définitions légales des violences sexistes et sexuelles - Connaître les principales données chiffrées sur le sujet - Comprendre les conséquences des violences sexistes et sexuelles - Connaître les responsabilités et obligations de l’employeur, les sanctions encourues et les procédures - Savoir accueillir la parole et orienter
Le cours réunira des intervenants de premier plan issus de différents domaines de la biologie des systèmes cancéreux, de la recherche sur le cancer et de la clinique. Les orateurs invités exposeront diverses approches pour l'analyse et l'interprétation des données omiques, d'imagerie et cliniques, en combinant les réseaux de signalisation avec des données moléculaires multi-échelles, et en les associant à des données cliniques.
Les thèmes abordés comprennent l'intégration et l'analyse de données génomiques multimodales, les algorithmes de prédiction de la sensibilité aux médicaments, l'identification de biomarqueurs et de facteurs de cancer, la stratification des patients, et les applications de la modélisation mathématique et de l'analyse d'images dans le domaine du cancer.
L'objectif du cours est de promouvoir une meilleure intégration des approches informatiques dans les laboratoires biologiques et cliniques et dans les cliniques. Nous voulons aider les participants à comprendre et à utiliser les approches d'intégration multimodale pour exploiter efficacement les différents types de données qui s'accumulent dans la plupart des laboratoires biologiques ou médicaux.
Le cours passera en revue les méthodes et outils actuels pour l'analyse et l'interprétation des données génomiques multimodales, en mettant l'accent sur la transcriptomique et la protéomique spatiales récentes, ainsi que sur des applications concrètes liées au cancer.
En particulier, le cours présentera des méthodes informatiques nous permettant d'approfondir notre compréhension de l'hétérogénéité des tumeurs, de tirer parti de l'intégration multimodale des données cliniques et omiques, et de concevoir des schémas de traitement personnalisés.
Centre de recherche - Paris - Amphitheatre Helene Martel-Massignac (BDD)
Vendredi 04 Octobre 2024    9:30
Invite par: Laura Cantini The Targeted Technological Action on Artificial Intelligence (ATC-IA) is organizing the second edition of its Symposium Artificial Intelligence in Biology and Health. It will be held on 4th October 2024 in the Emile ... Plus d'infos...
Tags: IA, Artificial intelligence
Annonce publiée le 04-03-2024
Institut Pasteur
Batiment: Emile Duclaux Salle: Lecture Hall
Mardi 15 Octobre 2024    11:30
Over the past two decades, there has been a significant shift in our understanding of the role of endocytosis and trafficking of signaling receptors. It has evolved from being viewed simply as a signal extinguisher (resulting in long-term attenuation) to being recognized as a sophisticated mechanism capable of delivering signals to specific cellular locations with precise timing. Therefore, endocytosis functions as a regulatory program that impacts various aspects of cell physiology, and we have evidence suggesting that alterations in this program may be causal and targetable in cancer. On the one hand, by exploiting the EGFR model system, we obtained confirmation that the integration of the two functions of endocytosis (sustainment and attenuation of signals) might be achieved, at least in part, at the plasma membrane (PM) by activation of different endocytic routes. Disruption of this balance appears to contribute significantly to cancer cell proliferation, invasion, and metastasis. On the other hand, our research has demonstrated the causal role of an endocytic protein, Epsin3 (EPN3), in breast cancer development, particularly in association with the emergence of partial epithelial-to-mesenchymal transition (pEMT), cancer stem cells, and invasive phenotypes. Increased E-cadherin endocytosis is the initial event driving EPN3-induced pEMT, that render cells more plastic and prone to metastatic dissemination. Importantly, inhibition of increased E-Cadherin endocytosis is capable of reversing EPN3-dependent invasiveness. The restricted expression of EPN3 in adult tissues, along with its overexpression in breast cancer, positions EPN3-drived endocytosis as a promising target for therapeutic intervention.