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Human Molecular Genetics Advance Access published online on February 24, 2009
Human Molecular Genetics, doi:10.1093/hmg/ddp086
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© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Sept5 deficiency exerts pleiotropic influence on affective behaviors and cognitive functions in mice

Go Suzuki1, Kathryn Harper2, Takeshi Hiramoto1, Takehito Sawamura1, MoonSook Lee1, Gina Kang1, Kenji Tanigaki3, Mahalah Buell4, Mark A. Geyer4, William S. Trimble5, Soh Agatsuma1 and Noboru Hiroi1,2,*

1 Department of Psychiatry and Behavioral Sciences, 1300 Morris Park Avenue, Bronx, NY 10461 2 Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461 3 Research Institute, Shiga Medical Center, 5-4-30 Moriyama, Moriyama-shi, Shiga 524-8524 Japan 4 Department of Psychiatry, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0804 5 Program in Cell Biology, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8

* Corresponding author: N. Hiroi, Ph.D., Department of Psychiatry and Behavioral Sciences, Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Golding 104, 1300 Morris Park Avenue, Bronx, NY 10461, Tel: 718-430-3124, Fax: 718-430-3125, E-mail: hiroi{at}aecom.yu.edu

Received January 16, 2009; Revised February 19, 2009; Accepted February 19, 2009

Deletion or duplication of the human chromosome 22q11.2 is associated with many behavioral traits and neuropsychiatric disorders, including autism spectrum disorders and schizophrenia. However, why phenotypes vary widely among individuals with identical deletions or duplications of 22q11.2 and which specific 22q11.2 genes contribute to these phenotypes are still poorly understood. Previous studies have identified a ~200 kb 22q11.2 region that contributes to behavioral phenotypes in mice. We tested the role of Septin 5 (Sept5), a gene encoded in the ~200 kb region, in affective behaviors, cognitive capacities, and motor activity. To evaluate the impact of genetic backgrounds on behavioral phenotypes of Sept5 deficiency, we used mice on two genetic backgrounds. Our data show that Sept5 deficiency decreased affiliative active social interaction, but this phenotypic expression was influenced by genetic backgrounds. By contrast, Sept5 deficiency decreased anxiety-related behavior, increased prepulse inhibition, and delayed acquisition of rewarded goal approach, independent of genetic background. These data suggest that Sept5 deficiency exerts pleiotropic effects on a select set of affective behaviors and cognitive processes and that genetic backgrounds could provide an epistatic influence on phenotypic expression.

The authors wish it to be known that, in their opinion, the first three authors (GS, KH and TH) should be regarded as joint First Authors.


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G. Suzuki, K. M. Harper, T. Hiramoto, B. Funke, M. Lee, G. Kang, M. Buell, M. A. Geyer, R. Kucherlapati, B. Morrow, et al.
Over-expression of a human chromosome 22q11.2 segment including TXNRD2, COMT and ARVCF developmentally affects incentive learning and working memory in mice
Hum. Mol. Genet., October 15, 2009; 18(20): 3914 - 3925.
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