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Mecp2 Truncation in Male Mice Promotes Affiliative Social Behavior.

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Title: Mecp2 Truncation in Male Mice Promotes Affiliative Social Behavior.
Authors: Pearson, B., Defensor, E., Pobbe, R., Yamamoto, L., Bolivar, V., Blanchard, D., Blanchard, R.
Source: Behavior Genetics. Mar2012, Vol. 42 Issue 2, p299-312. 14p. 2 Charts, 7 Graphs.
Subjects: Laboratory mice, Rett syndrome, Genotype-environment interaction, Syndromes in children, Autism, Age factors in cognition, Genetics
Abstract: Mouse models of Rett syndrome, with targeted mutations in the Mecp2 gene, show a high degree of phenotypic consistency with the clinical syndrome. In addition to severe and age-specific regression in motor and cognitive abilities, a variety of studies have demonstrated that Mecp2 mutant mice display impaired social behavior. Conversely, other studies indicate complex enhancements of social behavior in Mecp2 mutant mice. Since social behavior is a complicated accumulation of constructs, we performed a series of classic and refined social behavior tasks and revealed a relatively consistent pattern of enhanced pro-social behavior in hypomorphic Mecp2 mutant mice. Analyses of repetitive motor acts, and cognitive stereotypy did not reveal any profound differences due to genotype. Taken together, these results suggest that the mutations associated with Rett syndrome are not necessarily associated with autism-relevant social impairment in mice. However, this gene may be a valuable candidate for revealing basic mechanisms of affiliative behavior. [ABSTRACT FROM AUTHOR]
Copyright of Behavior Genetics is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Mecp2 Truncation in Male Mice Promotes Affiliative Social Behavior.
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  Data: <searchLink fieldCode="JN" term="%22Behavior+Genetics%22">Behavior Genetics</searchLink>. Mar2012, Vol. 42 Issue 2, p299-312. 14p. 2 Charts, 7 Graphs.
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  Data: <searchLink fieldCode="DE" term="%22Laboratory+mice%22">Laboratory mice</searchLink><br /><searchLink fieldCode="DE" term="%22Rett+syndrome%22">Rett syndrome</searchLink><br /><searchLink fieldCode="DE" term="%22Genotype-environment+interaction%22">Genotype-environment interaction</searchLink><br /><searchLink fieldCode="DE" term="%22Syndromes+in+children%22">Syndromes in children</searchLink><br /><searchLink fieldCode="DE" term="%22Autism%22">Autism</searchLink><br /><searchLink fieldCode="DE" term="%22Age+factors+in+cognition%22">Age factors in cognition</searchLink><br /><searchLink fieldCode="DE" term="%22Genetics%22">Genetics</searchLink>
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  Data: Mouse models of Rett syndrome, with targeted mutations in the Mecp2 gene, show a high degree of phenotypic consistency with the clinical syndrome. In addition to severe and age-specific regression in motor and cognitive abilities, a variety of studies have demonstrated that Mecp2 mutant mice display impaired social behavior. Conversely, other studies indicate complex enhancements of social behavior in Mecp2 mutant mice. Since social behavior is a complicated accumulation of constructs, we performed a series of classic and refined social behavior tasks and revealed a relatively consistent pattern of enhanced pro-social behavior in hypomorphic Mecp2 mutant mice. Analyses of repetitive motor acts, and cognitive stereotypy did not reveal any profound differences due to genotype. Taken together, these results suggest that the mutations associated with Rett syndrome are not necessarily associated with autism-relevant social impairment in mice. However, this gene may be a valuable candidate for revealing basic mechanisms of affiliative behavior. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Behavior Genetics is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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