"It is suggested that this mechanism of counteracting growth effects during embryogenesis evolved some 180 million years ago in a common ancestor to viviparous mammals after divergence from oviparous mammals (Das et al. 2012). Intriguingly, genomic imprinting also exists in the seed endosperm of flowering plants (angiosperms), demonstrating that this epigenetic mechanism evolved independently in the angiosperm and placental mammalian lineages, wherein the placenta and endosperm have analogous biological functions (de la Casa-Esperon & Sapienza 2003; Garnier et al. 2008; Kohler et al. 2012). "
[Show abstract][Hide abstract] ABSTRACT: The phenomenon of genomic imprinting, whereby a subset of mammalian genes display parent-of-origin-specific monoallelic expression, is one of the most active areas of epigenetics research. Over the past two decades, more than 100 imprinted mammalian genes have been identified, while considerable advances have been made in elucidating the molecular mechanisms governing imprinting. These studies have helped to unravel the epigenome – a separate layer of regulatory information contained in eukaryotic chromosomes that influences gene expression and phenotypes without involving changes to the underlying DNA sequence. Although most studies of genomic imprinting in mammals have focussed on mouse models or human biomedical disorders, there is burgeoning interest in the phenotypic effects of imprinted genes in domestic livestock species. In particular, research has focused on imprinted genes influencing foetal growth and development, which are associated with economically important production traits in cattle, sheep and pigs. These findings, when coupled with the data emerging from the various different livestock genome projects, have major implications for the future of animal breeding, health and management. Here, we review current scientific knowledge regarding genomic imprinting in livestock species and evaluate how this information can be used in modern livestock improvement programmes.
"While parent-of-origin-specific expression (e.g. due to genomic imprinting26) has been detected in triploid endosperm tissues,27–29 previous studies have found no evidence for parent-of-origin effects on gene expression in diploid vegetative tissues.22 "
[Show abstract][Hide abstract] ABSTRACT: Triploid F1 hybrids generated via reciprocal interploidy crosses between genetically distinct parental plants can display parent-of-origin effects on gene expression or phenotypes. Reciprocal triploid F1 isogenic plants generated from interploidy crosses in the same genetic background allow investigation on parent-of-origin-specific (parental) genome-dosage effects without confounding effects of hybridity involving heterozygous mutations. Whole-genome transcriptome profiling was conducted on reciprocal F1 isogenic triploid (3x) seedlings of A. thaliana. The genetically identical reciprocal 3x genotypes had either an excess of maternally inherited 3x(m) or paternally inherited 3x(p) genomes. We identify a major parent-of-origin-dependent genome-dosage effect on transcript levels, whereby 602 genes exhibit differential expression between the reciprocal F1 triploids. In addition, using methylation-sensitive DNA tiling arrays, constitutive and polymorphic CG DNA methylation patterns at CCGG sites were analysed, which revealed that paternal-excess F1 triploid seedling C(m)CGG sites are overall hypermethylated. However, no correlation exists between C(m)CGG methylation polymorphisms and transcriptome dysregulation between the isogenic reciprocal F1 triploids. Overall, our study indicates that parental genome-dosage effects on the transcriptome levels occur in paternal-excess triploids, which are independent of C(m)CGG methylation polymorphisms. Such findings have implications for understanding parental effects and genome-dosage effects on gene expression and phenotypes in polyploid plants.
DNA Research 11/2013; 21(2). DOI:10.1093/dnares/dst046 · 5.48 Impact Factor
"Many imprinted regions are either arranged in restrictive chromosomal areas or regulated as multigene clusters, indicating imprinted regions are contained as distinct structural domains. This organization may be related to the close association of imprinted domains to regions of the chromosome containing tandem repeats or transposable elements [9, 11, 15, 16]. It has further been suggested that these distinct imprinted domains could have a broader function to maintain genome integrity and assist in chromosome pairing, possibly contributing to the presence of such domains in diverse organisms . "
[Show abstract][Hide abstract] ABSTRACT: Genomic imprinting is a form of epigenetic inheritance whereby the regulation of a gene or chromosomal region is dependent on the sex of the transmitting parent. During gametogenesis, imprinted regions of DNA are differentially marked in accordance to the sex of the parent, resulting in parent-specific expression. While mice are the primary research model used to study genomic imprinting, imprinted regions have been described in a broad variety of organisms, including other mammals, plants, and insects. Each of these organisms employs multiple, interrelated, epigenetic mechanisms to maintain parent-specific expression. While imprinted genes and imprint control regions are often species and locus-specific, the same suites of epigenetic mechanisms are often used to achieve imprinted expression. This review examines some examples of the epigenetic mechanisms responsible for genomic imprinting in mammals, plants, and insects.
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