Abnormal behavior in mice mutant for the Disc1 binding partner, Dixdc1.

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Translational Psychiatry. 2011;1:e43. doi: 10.1038/tp.2011.41

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Abnormal behavior in mice mutant for the Disc1 binding partner, Dixdc1. Heberlein Lab

Kivimäe S, Martin P, Kapfhamer D, Ruan Y, Heberlein U, Rubenstein JL, Cheyette BN

Note: Research in this publication was not performed at Janelia.

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Abstract

Disrupted-in-Schizophrenia-1 (DISC1) is a genetic susceptibility locus for major mental illness, including schizophrenia and depression. The Disc1 protein was recently shown to interact with the Wnt signaling protein, DIX domain containing 1 (Dixdc1). Both proteins participate in neural progenitor proliferation dependent on Wnt signaling, and in neural migration independently of Wnt signaling. Interestingly, their effect on neural progenitor proliferation is additive. By analogy to Disc1, mutations in Dixdc1 may lead to abnormal behavior in mice, and to schizophrenia or depression in humans. To explore this hypothesis further, we generated mice mutant at the Dixdc1 locus and analyzed their behavior. Dixdc1(-/-) mice had normal prepulse inhibition, but displayed decreased spontaneous locomotor activity, abnormal behavior in the elevated plus maze and deficits in startle reactivity. Our results suggest that Dixdc1(-/-) mice will be a useful tool to elucidate molecular pathophysiology involving Disc1 in major mental illnesses.

PMID: 22832659 [PubMed - indexed for MEDLINE]

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Abnormal behavior in mice mutant for the Disc1 binding partner, Dixdc1.

Note: Research in this publication was not performed at Janelia.

Abstract

PMID: 22832659 [PubMed - indexed for MEDLINE]

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