Impulsive Choice in Mice Lacking Paternal Expression of<i>Grb10</i>Suggests Intragenomic Conflict in Behavior

Dent, Claire L.; Humby, Trevor; Lewis, Katie; Ward, Andrew; Fischer‐Colbrie, Reiner; Wilkinson, Lawrence S.; Wilkins, Jon F.; Isles, Anthony R

doi:10.1534/genetics.118.300898

Cited by 31 publications

(43 citation statements)

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“…Taken together, these findings suggest that paternal Grb10 may influence stability of social behavior. Nevertheless, although it is clear from the work here and others (Dent et al, 2018) that paternal Grb10 does impact on brain function generally, further work is required to determine the exact role played in social behavior.…”

Section: Clear Transitive Hierarchies In Individual Measures Of Sociamentioning

confidence: 72%

Detailed analysis of paternal knockout Grb10 mice suggests effects on stability of social behavior, rather than social dominance

Rienecker

Chavasse

Moorwood

et al. 2018

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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 currently 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 wildtype 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 on the stability of social behaviors, rather than dominance per se.

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Section: Clear Transitive Hierarchies In Individual Measures Of Sociamentioning

confidence: 72%

Detailed analysis of paternal knockout Grb10 mice suggests effects on stability of social behavior, rather than social dominance

Rienecker

Chavasse

Moorwood

et al. 2018

Preprint

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“…Grb10 in a number of brain regions (Garfield et al, 2011, Plagge et al, 2005 and cell types 8 (Dent et al, 2018), has led to the suggestion that they may have an antagonistic effect on 9 the control of behavior (Dent et al, 2018. This fits with the general idea 10 that genomic imprinting evolved as a consequence intragenomic conflict between maternal-11 and paternally-derived alleles arising as a consequence of kin-selection (Moore & Haig, 12 1991, Wilkins et al, 2016.…”

Section: Introductionmentioning

confidence: 87%

“…Grb10 have altered behavior (Rienecker et al, 2020), including a higher tolerance of delayed 9 rewards in a delay reinforcement task (DRT) (Dent et al, 2018). One suggestion is that 10 these changes reflect a role for Grb10 in regulating risk-taking behavior broadly (Wilkins & 11 Bhattacharya, 2019).…”

Section: Motivation For the Food Reward Is Not Altered In Grb10 +/P Mmentioning

confidence: 99%

“…The imprinted genes Grb10 and Nesp affect impulsive choice behavior in opposing 2 directions (Dent et al, 2016(Dent et al, , 2018. Mice lacking paternal Grb10 (Grb10 +/p ) prefer a larger, 3 but delayed reward to a smaller, but more immediate reward in the delayed reinforcement 4 task (DRT) (Dent et al, 2018). In contrast, mice lacking maternal Nesp (Nesp m/+ ) choose a 5 more immediate, smaller reward over a larger, but delayed reward in the DRT (Dent et al, 6 2016).…”

Section: Introductionmentioning

confidence: 99%

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Mice lacking paternal expression of imprintedGrb10are risk-takers

Dent

Rienecker

Ward

et al. 2020

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22The imprinted genes Grb10 and Nesp influence impulsive behavior on a delay discounting 23 task in an opposite manner. A recently developed theory suggests that this pattern of 24 behavior may be representative of predicted effects of imprinted genes on tolerance to risk. 25Here we examine whether mice lacking paternal expression of Grb10 show abnormal 26 behavior across a number of measures indicative of risk-taking. Although Grb10 +/p mice 27 show no difference from wild type littermates in their willingness to explore a novel 28 environment, their behavior on an explicit test of risk-taking, namely the Predator Odour 29Risk-Taking task, is indicative of an increased willingness to take risks. Follow-up tests 30 suggest that this risk-taking is not simply due to a general decrease in fear, or a general 31 increase in motivation for a food reward, but reflects a change in the trade-off between cost 32 and reward. These data, coupled with previous work on the impulsive behaviour of Grb10 +/p 33 mice in the delayed reinforcement task, and taken together with our work on mice lacking 34 maternal Nesp, suggest that maternally and paternally expressed imprinted genes oppositely 35 influence risk-taking behaviour as predicted. 36

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“…Even if we are close to a full understanding of the complement of imprinted genes in humans, it is not clear if and how expression from these loci affects language and communication. While the behavioral effects of some imprinted genes are starting to be dissected in more detail, the phenotypic effects of many imprinted genes remain unclear, and thus it is not known what effect (if any) they may have on linguistic behavior. More generally, much still remains unknown about the genetic basis of linguistic behavior, and while it is known that certain aspects of the language phenotype are highly heritable, the currently known variants can only explain a small portion of this .…”

Section: A New Approach To Understanding the Social Evolutionary Drivmentioning

confidence: 99%

Genomic Imprinting As a Window into Human Language Evolution

2019

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Humans spend large portions of their time and energy talking to one another, yet it remains unclear whether this activity is primarily selfish or altruistic. Here, it is shown how parent‐of‐origin specific gene expression—or “genomic imprinting”—may provide an answer to this question. First, it is shown why, regarding language, only altruistic or selfish scenarios are expected. Second, it is pointed out that an individual's maternal‐origin and paternal‐origin genes may have different evolutionary interests regarding investment into language, and that this intragenomic conflict may drive genomic imprinting which—as the direction of imprint depends upon whether investment into language is relatively selfish or altruistic—may be used to discriminate between these two possibilities. Third, predictions concerning the impact of various mutations and epimutations at imprinted loci on language pathologies are derived. In doing so, a framework is developed that highlights avenues for using intragenomic conflicts to investigate the evolutionary drivers of language.

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Impulsive Choice in Mice Lacking Paternal Expression ofGrb10Suggests Intragenomic Conflict in Behavior

Abstract: The imprinted gene Grb10 is expressed in the brain from the paternal copy only. Here, Dent et al. show that paternal Grb10 regulates impulsive choices, i.e. whether an animal chooses a smaller food reward...

Cited by 31 publications

References 33 publications

Detailed analysis of paternal knockout Grb10 mice suggests effects on stability of social behavior, rather than social dominance

Detailed analysis of paternal knockout Grb10 mice suggests effects on stability of social behavior, rather than social dominance

Mice lacking paternal expression of imprintedGrb10are risk-takers

Genomic Imprinting As a Window into Human Language Evolution

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