Title of article :
Genome-wide Generation and Systematic Phenotyping of Knockout Mice Reveals New Roles for Many Genes
Author/Authors :
Jacqueline K. White، نويسنده , , Anna-Karin Gerdin، نويسنده , , Natasha A. Karp، نويسنده , , Ed Ryder، نويسنده , , Marija Buljan، نويسنده , , James N. Bussell، نويسنده , , Jennifer Salisbury، نويسنده , , Simon Clare، نويسنده , , Neil J. Ingham، نويسنده , , Christine Podrini، نويسنده , , Richard Houghton، نويسنده , , Jeanne Estabel، نويسنده , , Joanna R. Bottomley، نويسنده , , David G. Melvin، نويسنده , , David Sunter، نويسنده , , Niels C. Adams، نويسنده , , The Sanger Institute Mouse Genetics Project، نويسنده , , David Tannahill، نويسنده , , Darren W. Logan، نويسنده , , Daniel G. MacArthur، نويسنده , , et al.، نويسنده ,
Issue Information :
هفته نامه با شماره پیاپی سال 2013
Pages :
13
From page :
452
To page :
464
Abstract :
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 We found that hitherto unpublished genes were as likely to reveal phenotypes as known genes, suggesting that novel genes represent a rich resource for investigating the molecular basis of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.
Journal title :
CELL
Serial Year :
2013
Journal title :
CELL
Record number :
1021820
Link To Document :
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