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

Targeted ANP32E mutant mice do not demonstrate obvious movement defects

Peiyan Wong  1 , Vonny I Leo, Meijun Low, Tak W Mak, Xiaodong Zhang, Patrick T Reilly
Affiliations

Targeted ANP32E mutant mice do not demonstrate obvious movement defects

Peiyan Wong et al. PLoS One. .

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.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. ANP32E-deficient mice perform normally on balance beam assay.
Mice were assayed, on light aversion balance beam across a 12 mm diameter dowel (panels A–C) and a 6 mm diameter dowel (panels D–F), for crossing time (panel A and D), number of slips (panels B and E) and number of grips (panels C and F). No statistically significant differences were detected between Anp32e −/− (KO, red) and Anp32e +/+ (WT, black).
Figure 2
Figure 2. No phenotypic difference of ANP32E-deficient mice in free stride gait.
Mouse gait analysis was performed on stationary runway and analysed for stance time (panel A), swing time (panel B) and stride time (panel C). Values for separate legs are presented separately. No statistically significant differences were detected by paired t-test analysis. FR, front right; FL, front left; RR, rear right; RL, rear right.
Figure 3
Figure 3. No phenotypic difference of ANP32E-deficient mice in forced stride gait.
Mouse gait analysis was performed on a treadmill and analysed for stance time (panel A), swing time (panel B) and stride time (panel C). Values for separate legs are presented separately. FR, front right; FL, front left; RR, rear right; RL, rear right.
Figure 4
Figure 4. ANP32E-deficient mice do not show defects in grip strength.
Mice were analysed for grip strength of front paws, hind paws, and total grip strength. No statistically significant differences were noted by paired t-test analysis.
See this image and copyright information in PMC

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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.