Large-scale neuroanatomical study uncovers 198 gene associations in mouse brain morphogenesis

Stephan C. Collins, Anna Mikhaleva, Katarina Vrcelj, Valerie E. Vancollie, Christel Wagner, Nestor Demeure, Helen Whitley, Meghna Kannan, Rebecca Balz, Lauren F. E. Anthony, Andrew Edwards, Hervé Moine, Jacqueline K. White, David J. Adams, Alexandre Reymond, Christopher J. Lelliott, Caleb Webber and Binnaz Yalcin ()
Additional contact information
Stephan C. Collins: Institut de Génétique et de Biologie Moléculaire et Cellulaire
Anna Mikhaleva: University of Lausanne
Katarina Vrcelj: University of Oxford
Valerie E. Vancollie: Wellcome Sanger Institute
Christel Wagner: Institut de Génétique et de Biologie Moléculaire et Cellulaire
Nestor Demeure: Institut de Génétique et de Biologie Moléculaire et Cellulaire
Helen Whitley: Institut de Génétique et de Biologie Moléculaire et Cellulaire
Meghna Kannan: Institut de Génétique et de Biologie Moléculaire et Cellulaire
Rebecca Balz: University of Lausanne
Lauren F. E. Anthony: Wellcome Sanger Institute
Andrew Edwards: Woodland View Hospital, NHS Ayrshire and Arran
Hervé Moine: Institut de Génétique et de Biologie Moléculaire et Cellulaire
Jacqueline K. White: Wellcome Sanger Institute
David J. Adams: Wellcome Sanger Institute
Alexandre Reymond: University of Lausanne
Christopher J. Lelliott: Wellcome Sanger Institute
Caleb Webber: University of Oxford
Binnaz Yalcin: Institut de Génétique et de Biologie Moléculaire et Cellulaire

Nature Communications, 2019, vol. 10, issue 1, 1-12

Abstract: Abstract Brain morphogenesis is an important process contributing to higher-order cognition, however our knowledge about its biological basis is largely incomplete. Here we analyze 118 neuroanatomical parameters in 1,566 mutant mouse lines and identify 198 genes whose disruptions yield NeuroAnatomical Phenotypes (NAPs), mostly affecting structures implicated in brain connectivity. Groups of functionally similar NAP genes participate in pathways involving the cytoskeleton, the cell cycle and the synapse, display distinct fetal and postnatal brain expression dynamics and importantly, their disruption can yield convergent phenotypic patterns. 17% of human unique orthologues of mouse NAP genes are known loci for cognitive dysfunction. The remaining 83% constitute a vast pool of genes newly implicated in brain architecture, providing the largest study of mouse NAP genes and pathways. This offers a complementary resource to human genetic studies and predict that many more genes could be involved in mammalian brain morphogenesis.

Date: 2019
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DOI: 10.1038/s41467-019-11431-2

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