Genomic imprinting as an adaptative model of developmental plasticity

Radford, Elizabeth J.; Ferrón, Sacri R.; Ferguson-Smith, Anne C.

doi:10.1016/j.febslet.2011.05.063

Cited by 58 publications

(45 citation statements)

References 86 publications

(114 reference statements)

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“…Often genome rearrangements that move novel genes into proximity with imprinted gene clusters can be invoked to explain some of the evolutionary fluidity of imprinting status. Within the genus Equus such mechanisms that result in rapid diversification of karyotypes are likely to be involved (44 We find support for the idea that genomic imprinting in the placenta may be an adaptive mechanism permitting plasticity of function in response to changing environmental conditions during gestation (45). The tissue specificity, incomplete silencing of the imprinted allele, and the interindividual variation in imprinting status that we have documented for many of the newly described imprinted genes may be other manifestations of flexibility in the design and construction of the mammalian placenta.…”

supporting

confidence: 50%

Paternally expressed genes predominate in the placenta

Wang

Miller

Harman

et al. 2013

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

146

143

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The discovery of genomic imprinting through studies of manipulated mouse embryos indicated that the paternal genome has a major influence on placental development. However, previous research has not demonstrated paternal bias in imprinted genes. We applied RNA sequencing to trophoblast tissue from reciprocal hybrids of horse and donkey, where genotypic differences allowed parent-of-origin identification of most expressed genes. Using this approach, we identified a core group of 15 ancient imprinted genes, of which 10 were paternally expressed. An additional 78 candidate imprinted genes identified by RNA sequencing also showed paternal bias. Pyrosequencing was used to confirm the imprinting status of six of the genes, including the insulin receptor ( INSR ), which may play a role in growth regulation with its reciprocally imprinted ligand, histone acetyltransferase-1 ( HAT1 ), a gene involved in chromatin modification, and lymphocyte antigen 6 complex, locus G6C, a newly identified imprinted gene in the major histocompatibility complex. The 78 candidate imprinted genes displayed parent-of-origin expression bias in placenta but not fetus, and most showed less than 100% silencing of the imprinted allele. Some displayed variability in imprinting status among individuals. This variability results in a unique epigenetic signature for each placenta that contributes to variation in the intrauterine environment and thus presents the opportunity for natural selection to operate on parent-of-origin differential regulation. Taken together, these features highlight the plasticity of imprinting in mammals and the central importance of the placenta as a target tissue for genomic imprinting.

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supporting

confidence: 50%

Paternally expressed genes predominate in the placenta

Wang

Miller

Harman

et al. 2013

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

146

143

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“…The mechanism by which IGs impact organ size is, however, not fully understood. It was proposed that IGs act at multiple levels to control energy homeostasis (Charalambous et al 2007;Radford et al 2011;Peters 2014) because IGs play critical roles in the development and function of key metabolic organs: brain, pituitary, adrenal, pancreas, muscle, white and brown adipose tissue, and liver. In this view, each IG is proposed to have a key function in the tissue(s) most affected by the corresponding mutant.…”

Section: Discussionmentioning

confidence: 99%

A systems-level approach to parental genomic imprinting: the imprinted gene network includes extracellular matrix genes and regulates cell cycle exit and differentiation

et al. 2015

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Genomic imprinting is an epigenetic mechanism that restrains the expression of~100 eutherian genes in a parent-of-originspecific manner. The reason for this selective targeting of genes with seemingly disparate molecular functions is unclear. In the present work, we show that imprinted genes are coexpressed in a network that is regulated at the transition from proliferation to quiescence and differentiation during fibroblast cell cycle withdrawal, adipogenesis in vitro, and muscle regeneration in vivo. Imprinted gene regulation is not linked to alteration of DNA methylation or to perturbation of monoallelic, parent-oforigin-dependent expression. Overexpression and knockdown of imprinted gene expression alters the sensitivity of preadipocytes to contact inhibition and adipogenic differentiation. In silico and in cellulo experiments showed that the imprinted gene network includes biallelically expressed, nonimprinted genes. These control the extracellular matrix composition, cell adhesion, cell junction, and extracellular matrix-activated and growth factor-activated signaling. These observations show that imprinted genes share a common biological process that may account for their seemingly diverse roles in embryonic development, obesity, diabetes, muscle physiology, and neoplasm.

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“…Imprinted genes play an important role in the control of growth and other processes, are widely expressed during prenatal development, and tend to be down-regulated after birth (6,12). The mechanisms through which imprinted genes control growth remain to be fully elucidated, although perturbations in imprinted gene dosage have recently been shown to alter the IGF1 signaling pathway (13,14).…”

mentioning

confidence: 99%

“…Genomic imprinting is a key modulator of developmental and physiological processes in mammals (6). Imprinting results in parental origin-specific gene expression and controls expression of a variety of genes often located in clusters, including proteincoding genes, retrotransposon-derived genes, and long noncoding RNAs (lncRNAs), as well as small-regulatory RNAs, such as microRNAs (miRNAs) and C/D-box small nucleolar RNAs (C/D snoRNAs) (7)(8)(9).…”

mentioning

confidence: 99%

Insulin and insulin-like growth factor 1 receptors are required for normal expression of imprinted genes

Boucher

Charalambous

Zarse

et al. 2014

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

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In addition to signaling through the classical tyrosine kinase pathway, recent studies indicate that insulin receptors (IRs) and insulinlike growth factor 1 (IGF1) receptors (IGF1Rs) can emit signals in the unoccupied state through some yet-to-be-defined noncanonical pathways. Here we show that cells lacking both IRs and IGF1Rs exhibit a major decrease in expression of multiple imprinted genes and microRNAs, which is partially mimicked by inactivation of IR alone in mouse embryonic fibroblasts or in vivo in brown fat in mice. This down-regulation is accompanied by changes in DNA methylation of differentially methylated regions related to these loci. Different from a loss of imprinting pattern, loss of IR and IGF1R causes down-regulated expression of both maternally and paternally expressed imprinted genes and microRNAs, including neighboring reciprocally imprinted genes. Thus, the unoccupied IR and IGF1R generate previously unidentified signals that control expression of imprinted genes and miRNAs through transcriptional mechanisms that are distinct from classical imprinting control.

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Genomic imprinting as an adaptative model of developmental plasticity

Cited by 58 publications

References 86 publications

Paternally expressed genes predominate in the placenta

Paternally expressed genes predominate in the placenta

A systems-level approach to parental genomic imprinting: the imprinted gene network includes extracellular matrix genes and regulates cell cycle exit and differentiation

Insulin and insulin-like growth factor 1 receptors are required for normal expression of imprinted genes

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