Literature search services are currently unavailable. During our hosting provider's UPS upgrade we experienced a hardware failure and are currently working to resolve the issue.

Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Functional genetic analysis of mouse chromosome 11.

Now that the mouse and human genome sequences are complete, biologists need systematic approaches to determine the function of each gene. 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 diseases. 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 chromosomes. 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.

Pubmed ID: 12955145


  • Kile BT
  • Hentges KE
  • Clark AT
  • Nakamura H
  • Salinger AP
  • Liu B
  • Box N
  • Stockton DW
  • Johnson RL
  • Behringer RR
  • Bradley A
  • Justice MJ



Publication Data

September 4, 2003

Associated Grants


Mesh Terms

  • Animals
  • Cardiovascular System
  • Chromosomes, Mammalian
  • Conserved Sequence
  • Ethylnitrosourea
  • Female
  • Gastrula
  • Genes, Lethal
  • Hematopoiesis
  • Humans
  • Infertility
  • Male
  • Mice
  • Mutagenesis
  • Mutagens
  • Mutation