"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.
"The effects on seed size thus likely result from an interplay between cytoplasmic effects, dosage effects, and genomic imprinting. Alternative theories have been proposed to explain the evolution of genomic imprinting and are reviewed elsewhere (Garnier et al., 2008; Moore and Mills, 2008). One of these proposes that genomic imprinting evolved to prevent parthenogenesis, explaining why gynogenotes and androgenotes fail to complete development (Barton et al., 1984; McGrath and Solter, 1984; Surani et al., 1984; Solter, 1988; Varmuza and Mann, 1994). "
[Show abstract][Hide abstract] ABSTRACT: Genomic imprinting results in monoallelic gene expression in a parent-of-origin-dependent manner. It is achieved by the differential epigenetic marking of parental alleles. Over the past decade, studies in the model systems Arabidopsis thaliana and maize (Zea mays) have shown a strong correlation between silent or active states with epigenetic marks, such as DNA methylation and histone modifications, but the nature of the primary imprint has not been clearly established for all imprinted genes. Phenotypes and expression patterns of imprinted genes have fueled the perception that genomic imprinting is specific to the endosperm, a seed tissue that does not contribute to the next generation. However, several lines of evidence suggest a potential role for imprinting in the embryo, raising questions as to how imprints are erased and reset from one generation to the next. Imprinting regulation in flowering plants shows striking similarities, but also some important differences, compared with the mechanisms of imprinting described in mammals. For example, some imprinted genes are involved in seed growth and viability in plants, which is similar in mammals, where imprinted gene regulation is essential for embryonic development. However, it seems to be more flexible in plants, as imprinting requirements can be bypassed to allow the development of clonal offspring in apomicts.
The Plant Cell 02/2011; 23(1):16-26. DOI:10.1105/tpc.110.081018 · 9.58 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The Dc8 gene of carrot (Daucus carota L.) shows differential expression during embryo development. Changes in methylation patterns of a segment of about 500 bp (from base +120 to base -446) of Dc8 allele 6 were investigated by treating genomic DNA, extracted from embryogenic callus at different stages of development, with sodium bisulfite to modify nonmethylated cytosines. Following asymmetric (strand-specific) amplification, base sequences for samples from each developmental stage were determined for each strand directly from the PCR products or from cloned PCR products. Different methylation patterns were detected in the two strands. The 5' to 3' sense (coding) strand was almost completely nonmethylated, whereas almost all the cytosines in the 3' to 5' (template) strand were methylated. By 71 days after transfer to embryo-inducing medium, few methylcytosines remained; those that were present were generally near the TATA box or in a region beyond -300. The cytosines that were methylated were not limited to CG or CNG sequences. The difference in the extent of methylation between the two complementary strands implies either that there is a mechanism for strand-specific methylation, or that complementary sequences can differ greatly in sensitivity to bisulfite treatment or PCR amplification.
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