Unexpected rescue of alpha-synuclein and multimerin1 deletion in C57BL/6JOlaHsd mice by beta-adducin knockout

Transgenic Res. 2006 Apr;15(2):255-9. doi: 10.1007/s11248-006-0003-6.

Abstract

Uniform genetic background of inbred mouse strains is essential in experiments with genetically modified mice. In order to assess Add2 (beta-adducin) function, its null mutation was produced in embryonic stem cells derived from 129Sv mouse and the subsequently obtained mouse mutants were backcrossed for 6 generations with C57BL/6JOlaHsd strain. Comparison of brain proteins between mutated and control animals by two-dimensional gels linked to mass spectroscopy analysis showed expression of Snca (alpha-synuclein) in the mutated animals, but unexpectedly not in the control C57BL/6JOlaHsd mice. Comparison between C57BL/6JOlaHsd and C57BL/6NCrl mice confirmed the presence of a deletion encompassing Snca and in addition Mmrn1 (multimerin1) loci in C57BL/6JOlaHsd strain. The segregation of mutated Add2 together with an adjacent part of the chromosome 6 derived from 129Sv mice, rescued the loss of these two genes in knockout mice on C57BL/6JOlaHsd background. The fact that Add2 knockout was compared with the C57BL/6JOlaHsd mouse strain, which is actually a double knockout of Snca and Mmrn1 emphasizes a need for information provided by commercial suppliers and of exact denominations of substrains used in research.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Proteins / deficiency
  • Blood Proteins / genetics*
  • Calmodulin-Binding Proteins / deficiency
  • Calmodulin-Binding Proteins / genetics*
  • Gene Deletion*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • alpha-Synuclein / deficiency
  • alpha-Synuclein / genetics*

Substances

  • Blood Proteins
  • Calmodulin-Binding Proteins
  • adducin
  • alpha-Synuclein
  • multimerin