Two new mouse chromosome 11 balancers

Genomics. 2004 Feb;83(2):303-10. doi: 10.1016/j.ygeno.2003.08.011.

Abstract

Segmental inversions causing recombination suppression are an essential feature of balancer chromosomes. Meiotic crossing over between homologous chromosomes within an inversion interval will lead to nonviable gametes, while gametes generated from recombination events elsewhere on the chromosome will be unaffected. This apparent recombination suppression has been widely exploited in genetic studies in Drosophila to maintain and analyze stocks carrying recessive lethal mutations. Balancers are particularly useful in mutagenesis screens since they help to establish the approximate genomic location of alleles of genes causing phenotypes. Using the Cre-loxP recombination system, we have constructed two mouse balancer chromosomes carrying 8- and 30-cM inversions between Wnt3 and D11Mit69 and between Trp53 and EgfR loci, respectively. The Wnt3-D11Mit69 inversion mutates the Wnt3 locus and is therefore homozygous lethal. The Trp53-EgfR inversion is homozygous viable, since the EgfR locus is intact and mutations in p53 are homozygous viable. A dominantly acting K14-agouti minigene tags both rearrangements, which enables these balancer chromosomes to be visibly tracked in mouse stocks. With the addition of these balancers to the previously reported Trp53-Wnt3 balancer, most of mouse chromosome 11 is now available in balancer stocks.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Chromosome Inversion*
  • Chromosomes*
  • ErbB Receptors / genetics
  • Genetic Engineering / methods
  • Mice
  • Mice, Transgenic
  • Molecular Probes
  • Proteins / genetics
  • Recombination, Genetic*
  • Tumor Suppressor Protein p53 / genetics
  • Wnt Proteins
  • Wnt3 Protein

Substances

  • Molecular Probes
  • Proteins
  • Tumor Suppressor Protein p53
  • WNT3 protein, human
  • Wnt Proteins
  • Wnt3 Protein
  • Wnt3 protein, mouse
  • ErbB Receptors