Journal
CELL
Volume 154, Issue 2, Pages 452-464Publisher
CELL PRESS
DOI: 10.1016/j.cell.2013.06.022
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Funding
- Wellcome Trust [098051, RG45277 PCAG/116]
- Medical Research Council
- European Commission (EUMODIC) [LSHG-CT-2006-037188]
- NIH [EY08213, 5K08EY020530-02]
- Research to Prevent Blindness
- Australian Research Council [DP1092723]
- Cancer Research UK
- MRC [G0300212, MC_qA137918] Funding Source: UKRI
- Cancer Research UK [13031, 12401] Funding Source: researchfish
- Medical Research Council [G0300212, MC_qA137918] Funding Source: researchfish
- Australian Research Council [DP1092723] Funding Source: Australian Research Council
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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 We found that hitherto unpublished genes were as likely to reveal phenotypes as known genes, suggesting that novel genes represent a rich resource for investigating the molecular basis of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.
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