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Nature 425, 81-86 (4 September 2003) | doi:10.1038/nature01865; Received 26 March 2003; Accepted 10 June 2003

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Functional genetic analysis of mouse chromosome 11

Benjamin T. Kile1,4, Kathryn E. Hentges1,4, Amander T. Clark1,4, Hisashi Nakamura1, Andrew P. Salinger1, Bin Liu1, Neil Box1, David W. Stockton1, Randy L. Johnson2, Richard R. Behringer3, Allan Bradley1,5 & Monica J. Justice1

  1. Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
  2. Department of Biochemistry and Molecular Biology, University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA
  3. Department of Molecular Genetics, University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA
  4. These authors contributed equally to this work
  5. Present address: The Wellcome Trust Sanger Institute, Hinxton, Cambridge, CB10 1SA, UK

Correspondence to: Monica J. Justice1 Email: mjustice@bcm.tmc.edu

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Now that the mouse and human genome sequences are complete, biologists need systematic approaches to determine the function of each gene1, 2. A powerful way to discover gene function is to determine the consequence of mutations in living organisms. Large-scale production of mouse mutations with the point mutagen N-ethyl-N-nitrosourea (ENU) is a key strategy for analysing the human genome because mouse mutants will reveal functions unique to mammals, and many may model human diseases3. To examine genes conserved between human and mouse, we performed a recessive ENU mutagenesis screen that uses a balancer chromosome, inversion chromosome 11 (refs 4, 5). Initially identified in the fruitfly, balancer chromosomes are valuable genetic tools that allow the easy isolation of mutations on selected chromosomes6. Here we show the isolation of 230 new recessive mouse mutations, 88 of which are on chromosome 11. This genetic strategy efficiently generates and maps mutations on a single chromosome, even as mutations throughout the genome are discovered. The mutations reveal new defects in haematopoiesis, craniofacial and cardiovascular development, and fertility.

  1. Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
  2. Department of Biochemistry and Molecular Biology, University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA
  3. Department of Molecular Genetics, University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA
  4. These authors contributed equally to this work
  5. Present address: The Wellcome Trust Sanger Institute, Hinxton, Cambridge, CB10 1SA, UK

Correspondence to: Monica J. Justice1 Email: mjustice@bcm.tmc.edu