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Targeted ANP32E Mutant Mice Do Not Demonstrate Obvious Movement Defects

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...

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Detalles Bibliográficos
Autores principales: Wong, Peiyan, Leo, Vonny I., Low, Meijun, Mak, Tak W., Zhang, Xiaodong, Reilly, Patrick T.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652840/
https://www.ncbi.nlm.nih.gov/pubmed/23675506
http://dx.doi.org/10.1371/journal.pone.0063815
Descripción
Sumario: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.