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1. Identifying causative mechanisms linking early-life stress to psycho-cardio-metabolic multi-morbidity:the EarlyCause project

Author

Mariani, N. (Nicole), Borsini, A. (Alessandra), Cecil, C. A. (Charlotte A. M.), Felix, J. F. (Janine F.), Sebert, S. (Sylvain), Cattaneo, A. (Annamaria), Walton, E. (Esther), Milaneschi, Y. (Yuri), Cochrane, G. (Guy), Amid, C. (Clara), Rajan, J. (Jeena), Giacobbe, J. (Juliette), Sanz, Y. (Yolanda), Agusti, A. (Ana), Sorg, T. (Tania), Herault, Y. (Yann), Miettunen, J. (Jouko), Parmar, P. (Priyanka), Cattane, N. (Nadia), Jaddoe, V. (Vincent), Lotjonen, J. (Jyrki), Buisan, C. (Carme), Gonzalez Ballester, M. A. (Miguel A.), Piella, G. (Gemma), Gelpi, J. L. (Josep L.), Lamers, F. (Femke), Penninx, B. W. (Brenda W. J. H.), Tiemeier, H. (Henning), von Tottleben, M. (Malte), Thiel, R. (Rainer), Heil, K. F. (Katharina F.), Jarvelin, M.-R. (Marjo-Riitta), Pariante, C. (Carmine), Mansuy, I. M. (Isabelle M.), Lekadir, K. (Karim), Mariani, N. (Nicole), Borsini, A. (Alessandra), Cecil, C. A. (Charlotte A. M.), Felix, J. F. (Janine F.), Sebert, S. (Sylvain), Cattaneo, A. (Annamaria), Walton, E. (Esther), Milaneschi, Y. (Yuri), Cochrane, G. (Guy), Amid, C. (Clara), Rajan, J. (Jeena), Giacobbe, J. (Juliette), Sanz, Y. (Yolanda), Agusti, A. (Ana), Sorg, T. (Tania), Herault, Y. (Yann), Miettunen, J. (Jouko), Parmar, P. (Priyanka), Cattane, N. (Nadia), Jaddoe, V. (Vincent), Lotjonen, J. (Jyrki), Buisan, C. (Carme), Gonzalez Ballester, M. A. (Miguel A.), Piella, G. (Gemma), Gelpi, J. L. (Josep L.), Lamers, F. (Femke), Penninx, B. W. (Brenda W. J. H.), Tiemeier, H. (Henning), von Tottleben, M. (Malte), Thiel, R. (Rainer), Heil, K. F. (Katharina F.), Jarvelin, M.-R. (Marjo-Riitta), Pariante, C. (Carmine), Mansuy, I. M. (Isabelle M.), and Lekadir, K. (Karim)

Abstract

Introduction: Depression, cardiovascular diseases and diabetes are among the major non-communicable diseases, leading to significant disability and mortality worldwide. These diseases may share environmental and genetic determinants associated with multimorbid patterns. Stressful early-life events are among the primary factors associated with the development of mental and physical diseases. However, possible causative mechanisms linking early life stress (ELS) with psycho-cardio-metabolic (PCM) multi-morbidity are not well understood. This prevents a full understanding of causal pathways towards the shared risk of these diseases and the development of coordinated preventive and therapeutic interventions. Methods and analysis: This paper describes the study protocol for EarlyCause, a large-scale and inter-disciplinary research project funded by the European Union’s Horizon 2020 research and innovation programme. The project takes advantage of human longitudinal birth cohort data, animal studies and cellular models to test the hypothesis of shared mechanisms and molecular pathways by which ELS shapes an individual’s physical and mental health in adulthood. The study will research in detail how ELS converts into biological signals embedded simultaneously or sequentially in the brain, the cardiovascular and metabolic systems. The research will mainly focus on four biological processes including possible alterations of the epigenome, neuroendocrine system, inflammatome, and the gut microbiome. Life-course models will integrate the role of modifying factors as sex, socioeconomics, and lifestyle with the goal to better identify groups at risk as well as inform promising strategies to reverse the possible mechanisms and/or reduce the impact of ELS on multi-morbidity development in high-risk individuals. These strategies will help better manage the impact of multi-morbidity on human health and the associated risk.

Published
2021

2. Analysis of mammalian gene function through broad-based phenotypic screens across a consortium of mouse clinics

Author

Hrabe de Angelis, M. (M), Nicholson, G. (G), Selloum, M. (Mohammed), White, J. (J) K. (K), Morgan, H. (H), Ramirez-Solis, R. (R), Sorg, T. (Tania), Wells, S. (S), Fuchs, H. (H), Fray, M. (M), Adams, D. (D) J. (J), Adams, N. (N) C. (C), Adler, T. (T), Aguilar-Pimentel, A. (A), Ali-Hadji, D. (Dalila), Amann, G. (Grégory), Andre, P. (Philippe), Atkins, S. (S), Auburtin, A. (Aurélie), Ayadi, A. (Abdelkader), Becker, J. (Julien), Becker, L. (L), Bedu, E. (Elodie), Bekeredjian, R. (R), Birling, M. (Marie-Christine), Blake, A. (A), Bottomley, J. (J), Bowl, M. (M) R. (R), Brault, V. (Véronique), Busch, D. (D) H. (H), Bussell, J. (J) N. (N), Calzada-Wack, J. (J), Cater, H. (H), Champy, M. (Marie-France), Charles, P. (Philippe), Chevalier, C. (Claire), Chiani, F. (F), Codner, G. (G) F. (F), Combe, R. (R), Cox, R. (R), Dalloneau, E. (E), Dierich, A. (A), Di Fenza, A. (A), Doe, B. (B), Duchon, A. (Arnaud), Eickelberg, O. (O), Esapa, C. (C) T. (T), Fertak, L. (L) E. (E), Feigel, T. (T), Emelyanova, I. (I), Estabel, J. (J), Favor, J. (J), Flenniken, A. (A), Gambadoro, A. (A), Garrett, L. (L), Gates, H. (H), Gerdin, A. (A) K. (K), Gkoutos, G. (G), Greenaway, S. (S), Glasl, L. (L), Goetz, P. (P), Da Cruz, I. (I) G. (G), Gotz, A. (A), Graw, J. (J), Guimond, A. (Alain), Hans, W. (W), Hicks, G. (G), Holter, S. (S) M. (M), Hofler, H. (H), Hancock, J. (J) M. (M), Hoehndorf, R. (R), Hough, T. (T), Houghton, R. (R), Hurt, A. (A), Ivandic, B. (B), Jacobs, H. (Hugues), Jacquot, S. (Sylvie), Jones, N. (N), Karp, N. (N) A. (A), Katus, H. (H) A. (A), Kitchen, S. (S), Klein-Rodewald, T. (T), Klingenspor, M. (M), Klopstock, T. (T), Lalanne, V. (Valérie), Leblanc, S. (Sophie), Lengger, C. (C), le Marchand, E. (Elise), Ludwig, T. (T), Lux, A. (Aline), McKerlie, C. (C), Maier, H. (H), Mandel, J. (Jean-Louis), Marschall, S. (S), Mark, M. (Manuel), Melvin, D. (D) G. (G), Meziane, H. (Hamid), Micklich, K. (K), Mittelhauser, C. (C), Monassier, L. (Laurent), Moulaert, D. (David), Muller, S. (Stéphanie), Naton, B. (B), Neff, F. (F), Nolan, P. (P) M. (M), Nutter, L. (L) M. (M), Ollert, M. (M), Pavlovic, G. (Guillaume), Pellegata, N. (N) S. (S), Peter, E. (E), Petit-Demouliere, B. (Benoît), Pickard, A. (A), Podrini, C. (C), Potter, P. (P), Pouilly, L. (Laurent), Puk, O. (O), Richardson, D. (D), Rousseau, S. (Stéphane), Quintanilla-Fend, L. (L), Quwailid, M. (M) M. (M), Racz, I. (I), Rathkolb, B. (B), Riet, F. (Fabrice), Rossant, J. (J), Roux, M. (Michel), Rozman, J. (J), Ryder, E. (E), Salisbury, J. (J), Santos, L. (L), Schable, K. (K) H. (H), Schiller, E. (E), Schrewe, A. (A), Schulz, H. (H), Steinkamp, R. (R), Simon, M. (M), Stewart, M. (M), Stoger, C. (C), Stoger, T. (T), Sun, M. (M), Sunter, D. (D), Teboul, L. (L), Tilly, I. (I), Tocchini-Valentini, G. (G) P. (P), Tost, M. (M), Treise, I. (I), Vasseur, L. (Laurent), Velot, E. (E), Vogt-Weisenhorn, D. (D), Wagner, C. (Christel), Walling, A. (A), Wattenhofer-Donze, M. (Marie), Weber, B. (Bruno), Wendling, O. (Olivia), Westerberg, H. (H), Willershauser, M. (M), Wolf, E. (E), Wolter, A. (A), Wood, J. (J), Wurst, W. (W), Yildirim, A. (A) O. (O), Zeh, R. (R), Zimmer, A. (A), Zimprich, A. (A), Consortium, E. (Eumodic), Holmes, C. (C), Steel, K. (K) P. (P), Herault, Y. (Yann), Gailus-Durner, V. (V), Mallon, A. (A) M. (M), and Brown, S. (S) D. (D)

Subjects
Genetics, Male, Mice, Knockout, Heterozygote, Mutant, Homozygote, Aucun, Molecular Sequence Annotation, Biology, Phenotype, Mice, Inbred C57BL, Pleiotropy, ddc:570, Mutation, Animals, Humans, Human genome, Female, Allele, Gene, Gene knockout, Genetic Association Studies
Abstract

The function of the majority of genes in the mouse and human genomes remains unknown. The mouse embryonic stem cell knockout resource provides a basis for the characterization of relationships between genes and phenotypes. The EUMODIC consortium developed and validated robust methodologies for the broad-based phenotyping of knockouts through a pipeline comprising 20 disease-oriented platforms. We developed new statistical methods for pipeline design and data analysis aimed at detecting reproducible phenotypes with high power. We acquired phenotype data from 449 mutant alleles, representing 320 unique genes, of which half had no previous functional annotation. We captured data from over 27,000 mice, finding that 83% of the mutant lines are phenodeviant, with 65% demonstrating pleiotropy. Surprisingly, we found significant differences in phenotype annotation according to zygosity. New phenotypes were uncovered for many genes with previously unknown function, providing a powerful basis for hypothesis generation and further investigation in diverse systems. Comment in : Genetic differential calculus. [Nat Genet. 2015] Comment in : Scaling up phenotyping studies. [Nat Biotechnol. 2015]

Published
2015

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