JK White, A-K Gerdin, NA Karp, E Ryder, M Buljan, JN Bussell, J Salisbury, S Clare, NJ Ingham, C Podrini, R Houghton, J Estabel, JR Bottomley, DG Melvin, D Sunter, NC Adams, Sanger Institute Mouse Genetics Project, D Tannahill, DW Logan, DG Macarthur, J Flint, VB Mahajan, SH Tsang, I Smyth, FM Watt, WC Skarnes, G Dougan, DJ Adams, R Ramirez-Solis, A Bradley, KP Steel
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Mutations in whole organisms are powerful ways of interrogating gene function in a realistic context. We describe a program, the Sanger Institute Mouse Genetics Project, that provides a step toward the aim of knocking out all genes and screening each line for a broad range of traits. We found that hitherto unpublished genes were as likely to reveal phenotypes as known genes, suggesting that novel genes represent a rich resource for investigating the molecular basis of disease. We found many unexpected phenotypes detected only because we screened for them, emphasizing the value of screening all mutants for a wide range of traits. Haploinsufficiency and pleiotropy were both surprisingly common. Forty-two percent of genes were essential for viability, and these were less likely to have a paralog and more likely to contribute to a protein complex than other genes. Phenotypic data and more than 900 mutants are openly available for further analysis. PAPERCLIP:
E-pub date: 
18 Jul 2013
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David Tannahill