Peg3 imprinted gene on proximal chromosome 7 encodes for a zinc finger protein

Kuroiwa, Yoshimi; Kaneko-Ishino, Tomoko; Kagitani, Fusako; Kohda, Takashi; Li, L L; Tada, Masako; Suzuki, Rika; Yokoyama, Minesuke; Shiroishi, Toshihiko; Wakana, Shigeharu; Barton, Sheila C.; Ishino, Fumitoshi; Surani, M. Azim

doi:10.1038/ng0296-186

Cited by 238 publications

(204 citation statements)

References 27 publications

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“…With the restriction landmark genome scanning (RLGS) method, the paternally expressed mouse gene, SP2 (U2aJbp-rs), was isolated (Hatada et al, 1993;Hayashizaki et al, 1994), assigned to an imprinting region of chromosome 11, and possibly plays a role in the determination of body size. Another approach, a screening of the genome by means of the subtraction hybridization method made it possible to isolate two novel mouse paternally expressed genes: Pegl (paternally expressed gene 1), which was mapped to chromosome 6 (Kaneko-Ishino et aL, 1995), and the other, Peg3, mapped to the proximal region of chromosome 7 (Kuroiwa et aL, 1996). Until now, 4 mouse maternally expressing genes, lgf2r, H19, Mash2 and p57 ~w2 (Hatada and Mukai, 1995), and 10 paternally expressing genes, Mas,Igf2,Ins2,Snrpn,Zuf127,Peg3,Pegl,lnsl,CDC25Mm and SP2 have been identified (Table 1).…”

Section: Identification Of Imprinted Genesmentioning

confidence: 99%

Genomic imprinting and its relevance to genetic diseases

Niikawa

1996

Jap J Human Genet

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SummaryGenomic imprinting is a biological phenomenon determined by an evolutionally acquired, underlying system that may control harmonious development and growth in mammals. It is also relevant to some genetic disorders in man. In this article, lines of biological evidence of imprinting, characteristics of the mouse and human imprinted genes, and findings and mechanisms on the occurrence of several human imprinting disorders are reviewed.

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Section: Identification Of Imprinted Genesmentioning

confidence: 99%

Genomic imprinting and its relevance to genetic diseases

Niikawa

1996

Jap J Human Genet

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“…However, two classic studies examining mice with targeted mutations demonstrate that imprinted genes also influence maternal behaviours (Lefebvre et al 1998;Li et al 1999). Peg1 and Peg3 are both paternally expressed imprinted genes that were identified in a screen for novel imprinted genes (Kanekoishino et al 1995;Kuroiwa et al 1996). Both have enhancing effects on foetal growth and are highly expressed in the adult brain (Lefebvre et al 1998;Li et al 1999).…”

Section: The Pre-weaning Period and Mother-offspring Bondingmentioning

confidence: 99%

Genomic imprinting and the social brain

Isles

Davies

Wilkinson

2006

Phil. Trans. R. Soc. B

109

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Genomic imprinting refers to the parent-of-origin-specific epigenetic marking of a number of genes. This epigenetic mark leads to a bias in expression between maternally and paternally inherited imprinted genes, that in some cases results in monoallelic expression from one parental allele. Genomic imprinting is often thought to have evolved as a consequence of the intragenomic conflict between the parental alleles that occurs whenever there is an asymmetry of relatedness. The two main examples of asymmetry of relatedness are when there is partiality of parental investment in offspring (as is the case for placental mammals, where there is also the possibility of extended postnatal care by one parent), and in social groups where there is a sex-biased dispersal. From this evolutionary starting point, it is predicted that, at the behavioural level, imprinted genes will influence what can broadly be termed bonding and social behaviour. We examine the animal and human literature for examples of imprinted genes mediating these behaviours, and divide them into two general classes. Firstly, mother-offspring interactions (suckling, attachment and maternal behaviours) that are predicted to occur when partiality in parental investment in early postnatal offspring occurs; and secondly, adult social interactions, when there is an asymmetry of relatedness in social groups. Finally, we return to the evolutionary theory and examine whether there is a pattern of behavioural functions mediated by imprinted genes emerging from the limited data, and also whether any tangible predictions can be made with regards to the direction of action of genes of maternal or paternal origin.

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“…Targeted deletion of Peg3 in either pups or independently in the mother results in a complementary phenotype affecting pup growth, pup suckling/maternal milk letdown, and pup thermoregulation/maternal nest-building (11), showing that these interdependent behaviors are coregulated by the same imprinted locus. Peg3 is strongly expressed in both the developing embryo and the hypothalamus (9,12), which controls maternal care in the mouse; in light of these findings, it has been proposed that coadaptation between mother and offspring may also have been a factor in the evolution of imprinting in mammals.…”

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confidence: 99%

Genomic imprinting mediates sexual experience-dependent olfactory learning in male mice

Swaney

Curley

Champagne

et al. 2007

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

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Mammalian imprinted genes are generally thought to have evolved as a result of conflict between parents; however, recent knockout studies suggest that coadaptation between mother and offspring may have been a significant factor. We present evidence that the same imprinted gene that regulates mammalian maternal care and offspring development also regulates male sexual behavior and olfaction. We have shown that the behavior of male mice carrying a knockout of the imprinted gene Peg3 does not change with sexual experience and that the mice are consequently unable to improve their copulatory abilities or olfactory interest in female odor cues after mating experience. Forebrain activation, as indexed by female odor-induced c-Fos protein induction, fails to increase with sexual experience, providing a neural basis for the behavioral deficits that the male mice display. The behavioral and neural effects of the Peg3 knockout show that this imprinted gene has evolved to regulate multiple and varied aspects of reproduction, from male sexual behavior to female maternal care, and the development of offspring. Moreover, sexual experience-driven behavioral changes may represent an adaptive response that enables males to increase their reproductive potential over their lifespan, and the effects we have found suggest that the evolution of genomic imprinting has been influenced by coadaptation between males and females as well as between females and offspring.accessory olfactory system ͉ coadaptation ͉ mammalian brain ͉ reward ͉ sexual behavior T he expression of certain mammalian autosomal genes in a parent-of-origin fashion was first demonstrated in the 1980s and termed ''genomic imprinting'' (1); since then, close to 100 maternally and paternally expressed imprinted genes have been identified (2). Over the last 20 years, the essential roles that imprinted genes play in development, particularly that of the brain, have become clear (3, 4), suggesting that imprinted genes might have enabled the evolutionary expansion of the mammalian brain (5). Most imprinted genes are strongly expressed in the placenta (6) and are involved in regulating fetal development (7). These developmental roles, in particular those of Igf2, Igf2r, Igf2AS, and H19, have been cited as evidence to support the conflict theory for the evolution of genomic imprinting (8). This theory posits that imprinted genes evolved with placentation in mammals as a result of parental conflict over offspring investment. The fetus/placenta is a genetically half-paternal structure that provides the father with an opportunity to manipulate the mother's investment in his offspring to the possible detriment of her potential future offspring. Thus, paternally expressed genes are predicted to enhance offspring growth, whereas maternally expressed genes are predicted to resist this as a result of an evolutionary ''arms race'' over levels of investment in offspring. However, work by our group on the paternally expressed gene Peg3 has shown that as well as regulating pup development...

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Peg3 imprinted gene on proximal chromosome 7 encodes for a zinc finger protein

Cited by 238 publications

References 27 publications

Genomic imprinting and its relevance to genetic diseases

Genomic imprinting and its relevance to genetic diseases

Genomic imprinting and the social brain

Genomic imprinting mediates sexual experience-dependent olfactory learning in male mice

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