Chromatin mechanisms in genomic imprinting

Kacem, Slim; Feil, Robert

doi:10.1007/s00335-009-9223-4

Cited by 123 publications

(76 citation statements)

References 127 publications

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“…Several of the trans-acting factors that control imprinting maintenance are organized in multi-protein complexes (Kacem and Feil, 2009;Kelsey and Feil, 2013). The composition and/or efficiency of such complexes may be compromised in hybrids due to polymorphisms, which could, for instance, interfere with stabilizing proteinprotein interactions.…”

Section: Differences Between the Parental Genomes Affect Imprinted Gementioning

confidence: 99%

Imprinted gene expression in hybrids: perturbed mechanisms and evolutionary implications

2014

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Diverse mechanisms contribute to the evolution of reproductive barriers, a process that is critical in speciation. Amongst these are alterations in gene products and in gene dosage that affect development and reproductive success in hybrid offspring. Because of its strict parent-of-origin dependence, genomic imprinting is thought to contribute to the aberrant phenotypes observed in interspecies hybrids in mammals and flowering plants, when the abnormalities depend on the directionality of the cross. In different groups of mammals, hybrid incompatibility has indeed been linked to loss of imprinting. Aberrant expression levels have been reported as well, including imprinted genes involved in development and growth. Recent studies in humans emphasize that genetic diversity within a species can readily perturb imprinted gene expression and phenotype as well. Despite novel insights into the underlying mechanisms, the full extent of imprinted gene perturbation still remains to be determined in the different hybrid systems. Here we review imprinted gene expression in intra-and interspecies hybrids and examine the evolutionary scenarios under which imprinting could contribute to hybrid incompatibilities. We discuss effects on development and reproduction and possible evolutionary implications.

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Section: Differences Between the Parental Genomes Affect Imprinted Gementioning

confidence: 99%

Imprinted gene expression in hybrids: perturbed mechanisms and evolutionary implications

2014

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“…either from the maternal or the paternal allele (for review: [1]). At the molecular level, the expression of genes within imprinted regions is influenced by specific patterns of DNA methylation, changes in chromatin structure, and post-translational histone modifications, collectively designated as epigenetic regulation (for review: [2,3]). So far, more than 90 human genes have been confirmed to be imprinted, but there are probably more based on bioinformatics predictions Their programming is subject to an imprinting cycle during life which leads to a reprogramming at each generation (for review: [4,5]).…”

Section: Introductionmentioning

confidence: 99%

Congenital imprinting disorders: Application of multilocus and high throughput methods to decipher new pathomechanisms and improve their management

Soellner

Monk

Rezwan

et al. 2015

Molecular and Cellular Probes

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Imprinting disorders (IDs) are a group of congenital diseases affecting growth, development and metabolism. They are caused by changes in the allele-specific regulation ("epigenetic mutation") or in the genomic sequence ("genetic mutation") of imprinted genes. Currently molecular tests in ID patients are generally restricted to single loci classically associated with the disease, but this approach limits diagnostic yield, because of the molecular and clinical heterogeneity between IDs. From the technical point of view, these limitations are aggravated by the lack of standardization in testing methodology, in the DNA sequences tested, and in clinical inclusion criteria prompting testing.However, an increasing number of new studies show that these problems can be addressed by the use of new tests targeting multiple loci and/or a total exome and genome analysis.The rapid development of efficient and high-throughput molecular techniques and their applications in research and diagnostics in the last decade have led to an impressive increase of knowledge on IDs and their basic pathomechanisms. In combination with the improvement of data recording and documentation, the diagnostic strategies are increasingly based on standardized protocols, and thereby provide the backbone for directed counselling, more personalized management, and new therapeutic approaches.

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“…In contrast to the above, a small percentage of "CpG" dinucleotides are clustered in regions termed "CpG islands", many of which surround gene promoters, the transcription start sites, and/or first exons [16]. Some 85-90% of such islands remain constitutively free of DNA methylation with the remainder associated with transcriptional silencing involved in X-chromosome inactivation [2,17], genomic imprinting [18], and transposable elements inhibition [2]. Some promoter islands in other gene types can also be mosaically methylated in normal tissues, especially those with less CpG density (or what have been referred to as "intermediate density" islands) [1].…”

Section: Dna Methylationmentioning

confidence: 99%

Cancer epigenetics: linking basic biology to clinical medicine

2011

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Cancer evolution at all stages is driven by both epigenetic abnormalities as well as genetic alterations. Dysregulation of epigenetic control events may lead to abnormal patterns of DNA methylation and chromatin configurations, both of which are critical contributors to the pathogenesis of cancer. These epigenetic abnormalities are set and maintained by multiple protein complexes and the interplay between their individual components including DNA methylation machinery, histone modifiers, particularly, polycomb (PcG) proteins, and chromatin remodeling proteins. Recent advances in genome-wide technology have revealed that the involvement of these dysregulated epigenetic components appears to be extensive. Moreover, there is a growing connection between epigenetic abnormalities in cancer and concepts concerning stem-like cell subpopulations as a driving force for cancer. Emerging data suggest that aspects of the epigenetic landscape inherent to normal embryonic and adult stem/ progenitor cells may help foster, under the stress of chronic inflammation or accumulating reactive oxygen species, evolution of malignant subpopulations. Finally, understanding molecular mechanisms involved in initiation and maintenance of epigenetic abnormalities in all types of cancer has great potential for translational purposes. This is already evident for epigenetic biomarker development, and for pharmacological targeting aimed at reversing cancerspecific epigenetic alterations.

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Chromatin mechanisms in genomic imprinting

Cited by 123 publications

References 127 publications

Imprinted gene expression in hybrids: perturbed mechanisms and evolutionary implications

Imprinted gene expression in hybrids: perturbed mechanisms and evolutionary implications

Congenital imprinting disorders: Application of multilocus and high throughput methods to decipher new pathomechanisms and improve their management

Cancer epigenetics: linking basic biology to clinical medicine

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