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12 results on '"Lindner, Loic"'

2. Changes in social behavior with MAPK2 and KCTD13/CUL3 pathways alterations in two new outbred rat models for the 16p11.2 syndromes with autism spectrum disorders

Author

Martin Lorenzo, Sandra, primary, Muniz Moreno, Maria del Mar, additional, Atas, Helin, additional, Pellen, Marion, additional, Nalesso, Valérie, additional, Raffelsberger, Wolfgang, additional, Prevost, Geraldine, additional, Lindner, Loic, additional, Birling, Marie-Christine, additional, Menoret, Séverine, additional, Tesson, Laurent, additional, Negroni, Luc, additional, Concordet, Jean-Paul, additional, Anegon, Ignacio, additional, and Herault, Yann, additional

Published
2023
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3. Changes in social behaviour with alterations of MAPK3 and KCTD13/CUL3 pathways in two new outbred rat models for the 16p11.2 syndromes with autism spectrum disorders

Author

Lorenzo, Sandra Martin, primary, Muniz Moreno, Maria Del Mar, additional, Atas, Helin, additional, Pellen, Marion, additional, Nalesso, Valérie, additional, Raffelsberger, Wolfgang, additional, Prevost, Geraldine, additional, Lindner, Loic, additional, Birling, Marie-Christine, additional, Menoret, Séverine, additional, Tesson, Laurent, additional, Negroni, Luc, additional, Concordet, Jean-Paul, additional, Anegon, Ignacio, additional, and Herault, Yann, additional

Published
2023
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5. Changes in social behavior with MAPK2 and KCTD13/CUL3 pathways alterations in two new outbred rat models for the 16p11.2 syndromes with autism spectrum disorders.

Author

Lorenzo, Sandra Martin, del Mar Muniz Moreno, Maria, Atas, Helin, Pellen, Marion, Nalesso, Valérie, Raffelsberger, Wolfgang, Prevost, Geraldine, Lindner, Loic, Birling, Marie-Christine, Menoret, Séverine, Tesson, Laurent, Negroni, Luc, Concordet, Jean-Paul, Anegon, Ignacio, and Herault, Yann

Subjects
AUTISM spectrum disorders, ANIMAL disease models, SOCIAL change, PHENOTYPIC plasticity, SEXUAL dimorphism, SELF-injurious behavior
Abstract

Copy number variations (CNVs) of the human 16p11.2 locus are associated with several developmental/neurocognitive syndromes. Particularly, deletion and duplication of this genetic interval are found in patients with autism spectrum disorders, intellectual disability and other psychiatric traits. The high gene density associated with the region and the strong phenotypic variability of incomplete penetrance, make the study of the 16p11.2 syndromes extremely complex. To systematically study the effect of 16p11.2 CNVs and identify candidate genes and molecular mechanisms involved in the pathophysiology, mouse models were generated previously and showed learning and memory, and to some extent social deficits. To go further in understanding the social deficits caused by 16p11.2 syndromes, we engineered deletion and duplication of the homologous region to the human 16p11.2 genetic interval in two rat outbred strains, Sprague Dawley (SD) and Long Evans (LE). The 16p11.2 rat models displayed convergent defects in social behavior and in the novel object test in male carriers from both genetic backgrounds. Interestingly major pathways affecting MAPK1 and CUL3 were found altered in the rat 16p11.2 models with additional changes in males compared to females. Altogether, the consequences of the 16p11.2 genetic region dosage on social behavior are now found in three different species: humans, mice and rats. In addition, the rat models pointed to sexual dimorphism with lower severity of phenotypes in rat females compared to male mutants. This phenomenon is also observed in humans. We are convinced that the two rat models will be key to further investigating social behavior and understanding the brain mechanisms and specific brain regions that are key to controlling social behavior. [ABSTRACT FROM AUTHOR]

Published
2023
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9. BIN1 Genetic Risk Factor for Alzheimer is Sufficient to Induce Early Structural Tract Alterations in Entorhinal-Hippocampal Area and Memory-Related Hippocampal Multi-Scale Impairments

Author

Daudin, Rachel, primary, Marechal, Damien, additional, Golgolab, Roxane, additional, Wang, Q, additional, Abe, Yoshifumi, additional, Tsurugizawa, TomoKazu, additional, Bourg, Nicolas, additional, Sartori, Maxime, additional, Loe-Mie, Yann, additional, Lipecka, J, additional, Guerrera, Chiara, additional, McKenzie, A, additional, Potier, Brigitte, additional, Dutar, Patrick, additional, Viard, Julia, additional, Lepagnol-Bestel, Aude-Marie, additional, Winkeler, Alexandra, additional, Uszynski, Ivy, additional, Hindié, Valérie, additional, Birling, Marie-Christine, additional, Lindner, Loic, additional, Chevalier, Claire, additional, Pavlovic, Guillaume, additional, Reiss, Martina, additional, Kranz, Harald, additional, Dupuis, Guillaume, additional, Leveque-Fort, Sandrine, additional, Diaz, J, additional, Davenas, Elisabeth, additional, Dembele, Doulaye, additional, Atas-Ozcan, Helin, additional, Laporte, J, additional, Thibault-Carpentier, Christelle, additional, Malissen, Bernard, additional, Rain, Jean-Christophe, additional, Poupon, Cyril, additional, Le Bihan, Denis, additional, Zhang, B, additional, Herault, Yann, additional, Ciobanu, Luisa, additional, and Simonneau, Michel, additional

Published
2021
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10. Atp6ap2 ablation in adult mice impairs viability through multiple organ deficiencies

Author

Wendling, Olivia, primary, Champy, Marie-France, additional, Jaubert, Solène, additional, Pavlovic, Guillaume, additional, Dubos, Aline, additional, Lindner, Loic, additional, Jacobs, Hugues, additional, Mark, Manuel, additional, Combe, Roy, additional, Da Cruz, Isabelle Goncalves, additional, Luche, Hervé, additional, Mudgett, John S., additional, Rosahl, Thomas, additional, Sorg, Tania, additional, Malissen, Marie, additional, Reilly, Patrick T., additional, and Hérault, Yann, additional

Published
2017
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11. Aneuploidy screening of embryonic stem cell clones by metaphase karyotyping and droplet digital polymerase chain reaction

Author

Codner, Gemma F., primary, Lindner, Loic, additional, Caulder, Adam, additional, Wattenhofer-Donzé, Marie, additional, Radage, Adam, additional, Mertz, Annelyse, additional, Eisenmann, Benjamin, additional, Mianné, Joffrey, additional, Evans, Edward P., additional, Beechey, Colin V., additional, Fray, Martin D., additional, Birling, Marie-Christine, additional, Hérault, Yann, additional, Pavlovic, Guillaume, additional, and Teboul, Lydia, additional

Published
2016
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12. CRISMERE Chromosome Engineering in Mouse and Rat.

Author

Schaeffer L, Lindner L, Pavlovic G, Hérault Y, and Birling MC

Subjects
Mice, Rats, Animals, Genomics, Mutation, Chromosomes, CRISPR-Cas Systems genetics, Genetic Engineering, DNA Copy Number Variations, Genome
Abstract

CRISPR/Cas9 technology is a versatile tool for engineering biology that has dramatically transformed our ability to manipulate genomes. In this protocol, we use its capacity to generate two double-strand breaks simultaneously, at precise positions in the genome, to generate mouse or rat lines with deletion, inversion, and duplication of a specific genomic segment. The technic is called CRISMERE for CRISpr-MEdiated REarrangement. This protocol describes the different steps to generate and validate the different chromosomal rearrangements that can be obtained with the technology. These new genetic configurations can be useful to model rare diseases with copy number variation, understand the genomic organization, or provide genetic tools (like balancer chromosome) to keep lethal mutations., (© 2023. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Published
2023
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