The paternally expressed gene Peg3 regulates sexual experience-dependent preferences for estrous odors.

Swaney, William T.; Curley, James P.; Champagne, Frances A.; Keverne, Eric B.

doi:10.1037/a0012706

Cited by 42 publications

(40 citation statements)

References 64 publications

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“…Peg3 +/− females show similar maternal behavioral deficits and increased maternal aggression (27,41,121). Behavioral reproductive defects are not confined to females: Peg3 +/− and Magel2 +/− males show an impaired response to female odors, resulting in reduced reproductive fitness (138,202,203).…”

Section: Leaving the Nestmentioning

confidence: 85%

“…Adult animals are underweight and hypophagic but have elevated adiposity, a secondary effect of dysregulated hypothalamic control of their metabolism (42). Peg3 mutations lead to delayed puberty in females, an anxiety-like phenotype, and a lack of the typical improvement in male sexual behavioral responses after sexual experience (27,41,42,202,203).…”

Section: Peg3 Domain: Mouse Chromosome 7 (Human Chromosome 19)mentioning

confidence: 99%

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Phenotypic Outcomes of Imprinted Gene Models in Mice: Elucidation of Pre- and Postnatal Functions of Imprinted Genes

Cleaton¹,

Edwards

Ferguson-Smith

2014

Annu. Rev. Genom. Hum. Genet.

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Genomic imprinting is an epigenetic process causing expression of a subset of genes in a parent-of-origin-specific manner. Among vertebrates, only therian mammals have been demonstrated to imprint, indicating that placentation and imprinting arose at similar time points in evolution and that imprinting may be involved in key mammal-specific processes. However, although several theories have been posited to explain the evolution of imprinting, each has shortcomings and none fully explains the wide variety of genes regulated by imprinting. In this review, we catalog the phenotypes associated with genetic mutation and overexpression at particular imprinted loci in order to consider the wide impact of imprinted genes on development. In addition to the well-described roles of imprinted genes in prenatal growth and placentation, more recent data emphasize that imprinted genes are critical for specific aspects of postnatal mammalian development involving adaptive processes, metabolism, and behavior.

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Section: Leaving the Nestmentioning

confidence: 85%

Section: Peg3 Domain: Mouse Chromosome 7 (Human Chromosome 19)mentioning

confidence: 99%

Phenotypic Outcomes of Imprinted Gene Models in Mice: Elucidation of Pre- and Postnatal Functions of Imprinted Genes

Cleaton¹,

Edwards

Ferguson-Smith

2014

Annu. Rev. Genom. Hum. Genet.

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“…Indeed, mate recognition is under the control of several imprinted genes. Males with Peg3 paternal deletions have impaired odor preferences for estrous females (Swaney et al 2008), reduced sexual behavior, and hypothalamic responses to female cues (Swaney et al 2007). Similarly, males with Magel2 paternal deletions show impaired preference for female odors (Mercer & Wevrick 2009).…”

Section: Functions Of Imprinted Genes In the Postnatal Brainmentioning

confidence: 99%

New Perspectives on Genomic Imprinting, an Essential and Multifaceted Mode of Epigenetic Control in the Developing and Adult Brain

Pérez

Rubinstein²,

Dulac

2016

Annu. Rev. Neurosci.

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Mammalian evolution entailed multiple innovations in gene regulation, including the emergence of genomic imprinting, an epigenetic regulation leading to the preferential expression of a gene from its maternal or paternal allele. Genomic imprinting is highly prevalent in the brain, yet, until recently, its central roles in neural processes have not been fully appreciated. Here, we provide a comprehensive survey of adult and developmental brain functions influenced by imprinted genes, from neural development and wiring to synaptic function and plasticity, energy balance, social behaviors, emotions, and cognition. We further review the widespread identification of parental biases alongside monoallelic expression in brain tissues, discuss their potential roles in dosage regulation of key neural pathways, and suggest possible mechanisms underlying the dynamic regulation of imprinting in the brain. This review should help provide a better understanding of the significance of genomic imprinting in the normal and pathological brain of mammals including humans.

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“…First, imprinted genes tend to have a clustered distribution in mammalian (15,18,19) and plant genomes (20), with the mammalian clustering appearing to be conserved in vertebrate evolution (21). Second, imprinted genes appear to modulate a limited number of types of traits, with most genes having effects on growth (especially in relation to the demand for maternal provisioning, often via the placenta) and/or behaviors (17,22), with behavioral effects being largely associated with parental and social behaviors (13,(23)(24)(25)(26)(27). Many of the theories for the evolution of genomic imprinting arise from or are strongly tied to this apparently limited range of phenotypes influenced by most imprinted genes.…”

mentioning

confidence: 99%

Evolution of genomic imprinting as a coordinator of coadapted gene expression

Wolf

2013

Proc. Natl. Acad. Sci. U.S.A.

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Genomic imprinting is an epigenetic phenomenon in which the expression of a gene copy inherited from the mother differs from that of the copy inherited from the father. Many imprinted genes appear to be highly interconnected through interactions mediated by proteins, RNA, and DNA. These kinds of interactions often favor the evolution of genetic coadaptation, where beneficially interacting alleles evolve to become coinherited. Here I demonstrate theoretically that the presence of gene interactions that favor coadaptation can also favor the evolution of genomic imprinting. Selection favors genomic imprinting because it coordinates the coexpression of positively interacting alleles at different loci. Evolution is expected to proceed through a scenario where selection builds associations between beneficial combinations of alleles and, if one locus evolves to become imprinted, it leads to selection for its interacting partners to match its pattern of imprinting. This process should favor the evolution of physical linkage between interacting genes and therefore may help explain why imprinted genes tend to be found in clusters. The model suggests that, whereas some genes are expected to evolve their imprinting status because selection directly favors a specific pattern of parent-of-origin-dependent expression, other genes may evolve imprinting as a coevolutionary response to match the expression pattern of their interacting partners. As a result, some genes will show phenotypic effects consistent with the predictions of models for the evolution of genomic imprinting (e.g., conflict models), but other genes may not, having simply evolved imprinting to follow the lead of their interacting partners.

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The paternally expressed gene Peg3 regulates sexual experience-dependent preferences for estrous odors.

Cited by 42 publications

References 64 publications

Phenotypic Outcomes of Imprinted Gene Models in Mice: Elucidation of Pre- and Postnatal Functions of Imprinted Genes

Phenotypic Outcomes of Imprinted Gene Models in Mice: Elucidation of Pre- and Postnatal Functions of Imprinted Genes

New Perspectives on Genomic Imprinting, an Essential and Multifaceted Mode of Epigenetic Control in the Developing and Adult Brain

Evolution of genomic imprinting as a coordinator of coadapted gene expression

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