Genomic imprinting in epigenetic of mammals

Platonov, E. S.; Isaev, D. A.

doi:10.1134/s1022795406090092

Cited by 6 publications

(6 citation statements)

References 114 publications

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“…epigenetic marking of germ cells' chromatin, sex-specific genomic imprinting; Narasimha et al 1997;Kimmins & Sassone-Corsi 2005;van de Lavoir et al 2006), (ii) somatic tissues to germ cells (path II, figure 1, e.g. somatic effects on gametogenesis, germ cell apoptosis and transfer of organelles, migration, mitosis and meiosis; Nakamura et al 1988;Barber et al 1991;Karagenc et al 1996;Johnson 2003;Bekaert et al 2004;Hashimoto et al 2004;Renault et al 2004;Platonov & Isaev 2006;Rutkowska & Badyaev 2008), and (iii) somatic tissues to somatic tissues (paths III and IV, e.g. effects of hormones, nutrients, transfer of symbionts and immunodefence factors, transfer of environment created or modified by parental activity; Odling-Smee et al 2003;Turner 2004;Weaver et al 2004;Moran 2007;Groothuis & Schwabl 2008).…”

Section: Parental Effects and Construction Of The Developmental Niche (A) Mechanisms Of Parental Effectsmentioning

confidence: 99%

Parental effects in ecology and evolution: mechanisms, processes and implications

Badyaev

Uller

2009

Phil. Trans. R. Soc. B

371

347

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As is the case with any metaphor, parental effects mean different things to different biologists—from developmental induction of novel phenotypic variation to an evolved adaptation, and from epigenetic transference of essential developmental resources to a stage of inheritance and ecological succession. Such a diversity of perspectives illustrates the composite nature of parental effects that, depending on the stage of their expression and whether they are considered a pattern or a process, combine the elements of developmental induction, homeostasis, natural selection, epigenetic inheritance and historical persistence. Here, we suggest that by emphasizing the complexity of causes and influences in developmental systems and by making explicit the links between development, natural selection and inheritance, the study of parental effects enables deeper understanding of developmental dynamics of life cycles and provides a unique opportunity to explicitly integrate development and evolution. We highlight these perspectives by placing parental effects in a wider evolutionary framework and suggest that far from being only an evolved static outcome of natural selection, a distinct channel of transmission between parents and offspring, or a statistical abstraction, parental effects on development enable evolution by natural selection by reliably transferring developmental resources needed to reconstruct, maintain and modify genetically inherited components of the phenotype. The view of parental effects as an essential and dynamic part of an evolutionary continuum unifies mechanisms behind the origination, modification and historical persistence of organismal form and function, and thus brings us closer to a more realistic understanding of life's complexity and diversity.

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Section: Parental Effects and Construction Of The Developmental Niche (A) Mechanisms Of Parental Effectsmentioning

confidence: 99%

Parental effects in ecology and evolution: mechanisms, processes and implications

Badyaev

Uller

2009

Phil. Trans. R. Soc. B

371

347

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“…Although imprinted genes account for only a small proportion of the mammalian genome, they play an important role in embryogenesis particularly in the formation of visceral structures and the nervous system [6]. Both mutations (causing DNA structure changes) and epigenetic modifications (affecting gene expression without altering the nucleotide DNA structure) in somatic cells disturb the expression of imprinted genes leading to malformations and syndromes caused by genomic imprinting defects.…”

Section: Assisted Reproductive Technology (Art) and Genomic Imprintingmentioning

confidence: 99%

“…However, the monoallelic expression of an imprinted gene is not absolute. Thus, a potential role of genomic imprinting in the differentiation of tissue types may be to determine the transcription rate of genes that influence growth through a fine balance between the expression of the two parental alleles [6].…”

Section: Introductionmentioning

confidence: 99%

“…In embryos containing only a paternal genome, reduced fetal growth and a proliferative extra-embryonic (placenta) growth occurs, whereas embryos containing a diploid set of maternal chromosomes maintain a relatively normal fetal growth pattern but exhibit poor extra-embryonic growth. The process of turning on and off genes, particularly developmental genes, is ongoing throughout the life cycle in mammals influenced by tissue specificity and timing [6,[19][20][21][22].…”

Section: Introductionmentioning

confidence: 99%

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Genomic imprinting disorders in humans: a mini-review

Butler

2009

J Assist Reprod Genet

188

134

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Mammals inherit two complete sets of chromosomes, one from the father and one from the mother, and most autosomal genes are expressed from both maternal and paternal alleles. Imprinted genes show expression from only one member of the gene pair (allele) and their expression are determined by the parent during production of the gametes. Imprinted genes represent only a small subset of mammalian genes that are present but not imprinted in other vertebrates. Genomic imprints are erased in both germlines and reset accordingly; thus, reversible depending on the parent of origin and leads to differential expression in the course of development. Genomic imprinting has been studied in humans since the early 1980's and accounts for several human disorders. The first report in humans occurred in Prader-Willi syndrome due to a paternal deletion of chromosome 15 or uniparental disomy 15 (both chromosome 15s from only one parent) and similar genetic disturbances were reported later in Angelman syndrome.

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“…The expression of imprinted genes is often tissue and stage specific. But, the monoallelic expression of an imprinted gene is not absolute and may incorporate differential transcription rates balanced between the two parental alleles [13]. Genes also appear to be clustered under the regulation of a single imprinting-controlling element which may involve higher order regulatory factors.…”

Section: Introductionmentioning

confidence: 99%

Examination of Global Methylation and Targeted Imprinted Genes in Prader- Willi Syndrome

Manzardo

2016

J Clin Epigenet

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Context Methylation changes observed in Prader-Willi syndrome (PWS) may impact global methylation as well as regional methylation status of imprinted genes on chromosome 15 (in cis) or other imprinted obesity-related genes on other chromosomes (in trans) leading to differential effects on gene expression impacting obesity phenotype unique to (PWS). Objective Characterize the global methylation profiles and methylation status for select imprinted genes associated with obesity phenotype in a well-characterized imprinted, obesity-related syndrome (PWS) relative to a cohort of obese and non-obese individuals. Design Global methylation was assayed using two methodologies: 1) enriched LINE-1 repeat sequences by EpigenDx and 2) ELISA-based immunoassay method sensitive to genomic 5-methylcytosine by Epigentek. Target gene methylation patterns at selected candidate obesity gene loci were determined using methylation-specific PCR. Setting Study participants were recruited as part of an ongoing research program on obesity-related genomics and Prader-Willi syndrome. Participants Individuals with non-syndromic obesity (N=26), leanness (N=26) and PWS (N=39). Results A detailed characterization of the imprinting status of select target genes within the critical PWS 15q11-q13 genomic region showed enhanced cis but not trans methylation of imprinted genes. No significant differences in global methylation were found between non-syndromic obese, PWS or non-obese controls. Intervention None. Main outcome measures Percentage methylation and the methylation index. Conclusion The methylation abnormality in PWS due to errors of genomic imprinting effects both upstream and downstream effectors in the 15q11-q13 region showing enhanced cis but not trans methylation of imprinted genes. Obesity in our subject cohorts did not appear to impact global methylation levels using the described methodology.

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Genomic imprinting in epigenetic of mammals

Cited by 6 publications

References 114 publications

Parental effects in ecology and evolution: mechanisms, processes and implications

Parental effects in ecology and evolution: mechanisms, processes and implications

Genomic imprinting disorders in humans: a mini-review

Examination of Global Methylation and Targeted Imprinted Genes in Prader- Willi Syndrome

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