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Targeted ANP32E mutant mice do not demonstrate obvious movement defects.

Peiyan Wong¹, Vonny I Leo, Meijun Low

¹Neuroscience and Behavioral Disorders Program, Duke-NUS Graduate Medical School, Singapore, Singapore.

|May 16, 2013

Summary

Studies on Anp32e (acidic nuclear phosphoprotein 32 family member E) suggest it impacts neuronal function. However, rigorous testing of Anp32e-deficient mice revealed no motor function deficits, questioning its role.

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Area of Science:

Neuroscience
Molecular Biology
Genetics

Background:

The ANP32 protein family is linked to neuronal function.
Previous studies suggested Anp32e influences fine motor control in mice.
Conflicting data emerged from a second targeted allele lacking neurological phenotypes.

Purpose of the Study:

To rigorously investigate the role of Anp32e in motor function.
To resolve discrepancies regarding Anp32e's neurological impact.

Main Methods:

Utilized a highly controlled cohort of ten-generation backcrossed, co-caged, sex-matched, littermate pairs.
Assayed for motor defects in ANP32E-deficient mice using stringent methods.

Main Results:

No phenotypic differences were observed in any motor function assays between ANP32E-deficient and control mice.
The findings contradict previous behavioral studies suggesting a role for Anp32e in motor control.

Conclusions:

ANP32E does not appear to have a significant effect on motor functions.
Genetic background differences likely explain the previously observed gene-trap phenomena.