Genomic imprinting in mammalian development: a parental tug-of-war

Moore, Tom

doi:10.1016/0168-9525(91)90040-w

Cited by 560 publications

(150 citation statements)

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“…The lack of imprinting of P1-driven IGF2 expression is still consistent with the parental conflict hypothesis of Moore and Haig (1991). Since P1 expression does not reach significant levels until after birth, there is no advantage for the maternal genome to inactivate the maternal IGF2 alleles.…”

Section: Discussionsupporting

confidence: 57%

“…This observation, coupled to the fact that these two genes are expressed from opposite parental alleles in the mouse led Moore and Haig (1991) to propose their 'parental conflict hypothesis' to explain the function of imprinting in mammals. This model proposes that imprinting in mammals evolved as a result of parental conflict in the pre-and postnatal allocation of a mother's resource to her offspring.…”

Section: Introductionmentioning

confidence: 96%

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Genomic imprinting of the insulin-like growth factor 2 gene in sheep

McLaren

Montgomery

1999

Mammalian Genome

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A number of genes in the human and mouse genomes are subject to genomic imprinting, with selective inactivation of one allele of a gene in a parent-of-origin specific manner. One of the first imprinted genes identified was the Insulin-like Growth Factor 2 gene (IGF2), which promotes growth of the fetus and is expressed from only the paternal allele in most tissues in both the mouse and human. The aim of this study was to establish the imprinting status of IGF2 in sheep (Ovis aries). Sheep provide an interesting model to study imprinting, owing to differences in their placental development and the fact that they have been subject to strong artificial selection for various production traits. We report the identification of a length polymorphism in the transcribed 3'-untranslated region of the ovine IGF2 gene. This polymorphism was used to map IGF2 to sheep Chromosome (Chr) 21 and demonstrate that IGF2 is indeed imprinted in sheep, being expressed from the paternal allele. We also report that the developmental switch from imprinted IGF2 expression in the fetal liver to biallelic IGF2 expression in the adult liver, which occurs in the human but not mouse, also occurs in sheep. Differences in male- and female-specific recombination values reported around the IGF2 locus in the human were also observed around the ovine IGF2 locus. The techniques developed in this study will enable the imprinting status of IGF2 to be assessed in a variety of tissues and stages of development in normal sheep.

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Section: Discussionsupporting

confidence: 57%

Section: Introductionmentioning

confidence: 96%

Genomic imprinting of the insulin-like growth factor 2 gene in sheep

McLaren

Montgomery

1999

Mammalian Genome

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“…Indeed, for the growth-related IGF2 and PEG1/MEST genes we provide evidence for their paternal expression being conserved in sheep. Our data on imprinting in sheep would support ''the conflict hypothesis'', a theory that predicts that imprinted genes that enhance embryonic growth are expressed off the paternally derived genome (Haig and Graham, 1991;Moore and Haig 1991). Our demonstration of imprinting in a mammal with a non-invasive placenta, however, seems not to fit hypotheses that say that imprinting restrains aggressive placentas from harming the pregnant mother (Hall 1990;Varmuza and Mann 1994).…”

Section: Figcontrasting

confidence: 60%

“…Although comparative studies have established that most of the imprinted rodent genes are parental allele-specifically expressed in humans as well (John and Surani 1996), and vice versa, it is not known whether genomic imprinting is conserved among other mammalian groups. Many theories have been developed that consider the evolution of genomic imprinting (Hurst 1997), possibly the most inclusive of these says that imprinting evolved because of the conflicting interests of maternal and paternal genes in relation to transfer of nutrients from the mother to her offspring during pre-and postnatal development (the ''conflict hypothesis'': Haig and Graham 1991;Moore and Haig 1991). It would be important to know to which extent genomic imprinting is conserved among eutherian mammals in order to evaluate this and other evolutionary theories of imprinting.…”

Section: Introductionmentioning

confidence: 99%

Genomic imprinting in ruminants: allele-specific gene expression in parthenogenetic sheep

et al. 1998

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Studies in the mouse have established that both parental genomes are essential for normal embryonic development. Parthenogenetic mouse embryos (which have two maternal genomes and no paternal genome), for example, are growth-retarded and die at early postimplantation stages. The distinct maternal and paternal contributions are mediated by genomic imprinting, an epigenetic mechanism by which the expression of certain genes is dependent on whether they are inherited from mother or father. Although comparative studies have established that many imprinted mouse (and rat) genes are allele-specifically expressed in humans as well (and vice versa), so far imprinting studies have not been performed in other mammalian species. When considering evolutionary theories of genomic imprinting, it would be important to know how widely it is conserved among placental mammals. We have investigated its conservation in a bovid ruminant, the domestic sheep, by comparing parthenogenetic and normal control embryos. Our study establishes that, like in the mouse, parthenogenetic development in sheep is associated with growth-retardation and does not proceed beyond early fetal stages. These developmental abnormalities are most likely caused by imprinted genes. We demonstrate that, indeed, like in mice and humans, the growth-related PEG1/MEST and Insulin-like Growth Factor 2 (IGF2) genes are expressed from the paternal chromosome in sheep. These observations suggest that genomic imprinting is conserved in a third, evolutionarily rather diverged group of placental mammals, the ruminants.

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“…Daher ist es nicht verwunderlich, dass viele der geprägten Gene in Wachstums-und Entwicklungsprozesse involviert sind. Tatsäch-lich haben mütterlich und väterlich exprimierte Gene in ihrer biologischen Rolle als Vermittler in der "Kampf-der-Geschlechter"-Hypothese ("battle of sexes", "conflict hypothesis") eine gegensätzliche Funktion in der Fetalperiode [19]: so fördern väter-lich geprägte Gene das fetale Wachstum, während mütterlich exprimierte Gene dasselbe unterdrücken. Auf molekularer Ebene wird die Regulation dieser Gene im Wesentlichen durch DNA-Methylierung, Chromatinstrukturen, posttranslationale Histonmodifikationen und MikroRNA vermittelt.…”

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