Abstract
Imprinted genes are highly expressed in monoaminergic regions of the midbrain and their functions in this area are thought to have an impact on mammalian social behaviors. One such imprinted gene is Grb10, of which the paternal allele is generally recognized as mediating social dominance behavior. However, there has been no detailed study of social dominance in Grb10 +/p mice. Moreover, the original study examined tube‐test behavior in isolated mice 10 months of age. Isolation testing favors more territorial and aggressive behaviors, and does not address social dominance strategies employed in group housing contexts. Furthermore, isolation stress impacts midbrain function and dominance related behavior, often through alterations in monoaminergic signaling. Thus, we undertook a systematic study of Grb10 +/p social rank and dominance behavior within the cage group, using a number of convergent behavioral tests. We examined both male and female mice to account for sex differences and tested cohorts aged 2, 6 and 10 months to examine any developments related to age. We found group‐housed Grb10 +/p mice do not show evidence of enhanced social dominance, but cages containing Grb10 +/p and wild‐type mice lacked the normal correlation between three different measures of social rank. Moreover, a separate study indicated isolation stress induced inconsistent changes in tube test behavior. Taken together, these data suggest future research on Grb10 +/p mice should focus on the stability of social behaviors, rather than dominance per se.
Highlights
Imprinted genes are defined by their monoallelic, parent-of-origin dependent expression originating from differential epigenetic marks established in the germline.[1]
The paternally expressed copy of the imprinted gene Grb[10] is expressed in the developing and adult brain, and we have previously established a potential link to social dominance in mice with disruption of the paternally inherited allele (Grb10+/p).[3]
Protein belonging to the small Grb7/Grb10/Grb[14] family.[4,5]. This protein has an inhibitory effect on signaling through receptor tyrosine kinases, including the insulin receptor and insulin-like growth factor receptor.[6]
Summary
Imprinted genes are defined by their monoallelic, parent-of-origin dependent expression originating from differential epigenetic marks established in the germline.[1]. Male Grb10+/p mice 10 months of age were previously reported to be significantly less likely to back down in the Lindzey tube test This correlated with an elevated incidence of facial barbering in cages containing Grb10+/p mutants.[3] Both measures are considered indicators of social dominance.[8,9,10] in the original study tube testing was not conducted within an animal's normal cage group, and took place after mice were isolated for an extended period to determine whether the barbering was self-inflicted.[3] Social isolation impacts midbrain function and dominance-related behaviors, often through alterations in monoaminergic signaling.[11,12] In periods of isolation between 14 and 28 days, this includes alterations in tyrosine hydroxylase transcription, and over 3 months this includes changes in epigenetic marks and writer/eraser activity in the midbrain.[11,13] Even short periods alter signaling and connectivity. We used convergent measures to assess dominance behavior in socially housed Grb10+/p mice, including the stranger- and social-encounter Lindzey tube tests, the urine marking test, and characterization of barbering behavior Both male and female cohorts were used to test for any sex differences. Our results indicate Grb10+/p mice are not more dominant, but may show a social instability phenotype
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