Targeted ANP32E mutant mice do not demonstrate obvious movement defects

PLoS One. 2013 May 13;8(5):e63815. doi: 10.1371/journal.pone.0063815. Print 2013.

Abstract

Background: The ANP32 family of proteins have been implicated in neuronal function through biochemical and cellular biology studies in neurons, as well as by recent behavioural studies of a gene-trapped loss-of-function mutation of Anp32e in mice, particularly with respect to fine motor function. A second targeted allele of the Anp32e, however, did not appear to demonstrate neurological phenotypes.

Methodology/principal findings: Using a stringently controlled cohort of ten-generation backcrossed, co-caged, sex-matched, littermate pairs, we assayed for potential motor defects in the targeted ANP32E-deficient mice. We found no phenotypic difference in any assays.

Conclusion: Since it is unlikely that the gene-trap is a more complete loss-of-function, our results suggest that ANP32E has no appreciable effect on motor functions and that genetic background differences most likely account for the gene-trap phenomena.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Animals
  • Female
  • Heterozygote
  • Homozygote
  • Male
  • Mice
  • Mice, Transgenic
  • Molecular Chaperones
  • Motor Activity / physiology*
  • Mutation*
  • Nerve Tissue Proteins / genetics*
  • Phenotype

Substances

  • Anp32e protein, mouse
  • Molecular Chaperones
  • Nerve Tissue Proteins

Grants and funding

This work was supported by funding from the Singhealth Research Foundation and the National Cancer Centre Singapore. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.