Impulsive choice in mice lacking paternal expression of Grb10 suggests intra-genomic conflict in behavior

Mapping Intimacies ◽

10.1101/281873 ◽

2018 ◽

Author(s):

Claire L. Dent ◽

Trevor Humby ◽

Katie Lewis ◽

Andrew Ward ◽

Reiner Fischer-Colbrie ◽

...

Keyword(s):

Germ Line ◽

Imprinted Genes ◽

Impulsive Choice ◽

Impulsive Behavior ◽

Parental Allele ◽

Genomic Conflict ◽

Epigenetic Events ◽

Contrasting Effect ◽

Brain And Behavior ◽

And Behavior

AbstractImprinted genes are expressed from one parental allele only as a consequence of epigenetic events that take place in the mammalian germ line and are thought to have evolved through intra-genomic conflict between parental alleles. We demonstrate, for the first time, oppositional effects of imprinted genes on brain and behavior. Specifically, here we show that mice lacking paternal Grb10 make fewer impulsive choices, with no dissociable effects on a separate measure of impulsive action. Taken together with previous work showing that mice lacking maternal Nesp55 make more impulsive choices this suggests that impulsive choice behavior is a substrate for the action of genomic imprinting. Moreover, the contrasting effect of these two genes suggests impulsive choices are subject to intra-genomic conflict and that maternal and paternal interests pull this behavior in opposite directions. Finally, these data may also indicate that an imbalance in expression of imprinted genes contributes to pathological conditions such as gambling and drug addiction, where impulsive behavior becomes maladaptive.

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Coming of Age

10.1093/oso/9780195314373.001.0001 ◽

2019 ◽

Cited By ~ 1

Author(s):

Cheryl L. Sisk ◽

Russell D. Romeo

Keyword(s):

Coming Of Age ◽

Laboratory Animals ◽

Impulsive Behavior ◽

Graduate Course ◽

Basic Principles ◽

Neural Underpinnings ◽

Brain And Behavior ◽

Upper Level ◽

And Behavior ◽

Adolescent Brain Development

The purpose of this book is to explore the neurobiology and psychobiology underlying puberty and adolescence. It tells the story of how contemporary neuroscience has come to make significant contributions to the understanding of a developmental period that used to be the sole purview of developmental psychologists and pediatric endocrinologists. The authors presume the reader will have a general understanding of the basic principles of neuroscience and psychology and have written this book to serve as an appropriate text for an upper-level undergraduate seminar or graduate course designed to probe puberty and adolescence more deeply from a psychobiological perspective. Topics covered in specific chapters include timing and regulation of reproductive maturation (puberty), mechanisms of adolescent brain development in laboratory animals and humans, neural underpinnings of higher risk-taking and impulsive behavior in adolescents, hormonal programming of social behaviors during adolescence, and effects of stress and drugs on the adolescent brain. The book ends with the authors’ perspective on some of the big questions about the adolescent brain and behavior that remain to be answered.

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Specific Differentially Methylated Domain Sequences Direct the Maintenance of Methylation at Imprinted Genes

Molecular and Cellular Biology ◽

10.1128/mcb.00981-06 ◽

2006 ◽

Vol 26 (22) ◽

pp. 8347-8356 ◽

Cited By ~ 18

Author(s):

Bonnie Reinhart ◽

Ariane Paoloni-Giacobino ◽

J. Richard Chaillet

Keyword(s):

Tandem Repeats ◽

Germ Line ◽

Gene Clusters ◽

Imprinted Genes ◽

Specific Expression ◽

Cpg Dinucleotides ◽

Parental Allele ◽

Epigenetic State ◽

Genomic Reprogramming ◽

Genomic Signal

ABSTRACT Landmark features of imprinted genes are differentially methylated domains (DMDs), in which one parental allele is methylated on CpG dinucleotides and the opposite allele is unmethylated. Genetic experiments in the mouse have shown that DMDs are required for the parent-specific expression of linked clusters of imprinted genes. To understand the mechanism whereby the differential methylation is established and maintained, we analyzed a series of transgenes containing DMD sequences and showed that imperfect tandem repeats from DMDs associated with the Snurf/Snrpn, Kcnq1, and Igf2r gene clusters govern transgene imprinting. For the Igf2r DMD the minimal imprinting signal is two unit copies of the tandem repeat. This imprinted transgene behaves identically to endogenous imprinted genes in Dnmt1o and Dnmt3L mutant mouse backgrounds. The primary function of the imprinting signal within the transgene DMD is to maintain, during embryogenesis and a critical period of genomic reprogramming, parent-specific DNA methylation states established in the germ line. This work advances our understanding of the imprinting mechanism by defining a genomic signal that dependably perpetuates an epigenetic state during postzygotic development.

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