Abstract

Usually, most of the genes are biallelically expressed but imprinted gene exhibit monoallelic expression based on their parental origin. Genomic imprinting exhibit differences in control between flowering plants and mammals, for instance, imprinted gene are specifically activated by demethylation, rather than targeted for silencing in plants and imprinted gene expression in plant which occur in endosperm. It also displays sexual dimorphism like differential timing in imprint establishment and RNA based silencing mechanism in paternally repressed imprinted gene. Within imprinted regions, the unusual occurrence and distribution of various types of repetitive elements may act as genomic imprinting signatures. Imprinting regulation probably at many loci involves insulator protein dependent and higher-order chromatin interaction, and/or non-coding RNAs mediated mechanisms. However, placenta-specific imprinting involves repressive histone modifications and non-coding RNAs. The higher-order chromatin interaction involves differentially methylated domains (DMDs) exhibiting sex-specific methylation that act as scaffold for imprinting, regulate allelic-specific imprinted gene expression. The paternally methylated differentially methylated regions (DMRs) contain less CpGs than the maternally methylated DMRs. The non-coding RNAs mediated mechanisms include C/D RNA and microRNA, which are invovled in RNA-guided post-transcriptional RNA modifications and RNA-mediated gene silencing, respectively. The maintenance and reprogramming of imprinting are not significantly affected by reduced expression of Dicer1 and the evolution of imprinting might be related to acquisition of DNMT3L (de novo methyltransferase 3L) by a common ancestor of eutherians and marsupials. The common feature among diverse imprinting control elements and evolutionary significance of imprinting need to be identified.   Key words: Genomic imprinting, differentially methylated regions (DMRs), non-coding RNA, imprinting evolution.

Highlights

  • Genomic imprinting is a germline-specific epigenetic modification of the genome that results in parent-oforigin-specific expression of a small subset of genes in offspring

  • DNA methylation is probably the more stable epigenetic mark in the embryo, which may be appropriate in this case for the imprint to survive in adulthood, while histone modifications may serve purpose in the short-lived placenta that is not required after birth

  • Dnmt1o could be attracted to the hemimethylated differentially methylated domains (DMDs) due to the arrangement of CpG dinucleotides, the imperfect repetitiveness, and a specific chromatin structure induced by the hemimethylated DMD

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Summary

Biotechnology and Molecular Biology Reviews

Most of the genes are biallelically expressed but imprinted gene exhibit monoallelic expression based on their parental origin. Genomic imprinting exhibit differences in control between flowering plants and mammals, for instance, imprinted gene are activated by demethylation, rather than targeted for silencing in plants and imprinted gene expression in plant which occur in endosperm. It displays sexual dimorphism like differential timing in imprint establishment and RNA based silencing mechanism in paternally repressed imprinted gene. Placentaspecific imprinting involves repressive histone modifications and non-coding RNAs. The higher-order chromatin interaction involves differentially methylated domains (DMDs) exhibiting sex-specific methylation that act as scaffold for imprinting, regulate allelic-specific imprinted gene expression.

INTRODUCTION
Fate of imprints during mammalian life cycle
Expression profiles of Megs and Pegs in mammalian life cycle
Differential characteristics between plants and animals
Sexual dimorphism of imprinting
Imprinting in placenta
REPETITIVE ELEMENT ROLE IN IMPRINTING
Retrotransposable element
Tandem repeats
Long repeat motifs
Direct tandem repeats
EPIGENETIC MODIFICATIONS
DNA methylation
Cis acting DNA signal for methylation
Polycomb group proteins
Chromatin modifying factor
Chromatin remodeling factor
Regulation of CTCF
Histone modifications
Interactions of epigenetic modifications
REGULATORY MECHANISM
Imprinting centre and its characteristics
Different mechanisms involved in regulation
Looping model
Dual role of ICs
Role of dicer in imprinting
Conflict hypothesis or kinship theory
Complementation hypothesis
Barrier to parthenogenesis in mammals
Host defense mechanism
Ovarian time bomb theory
Novel placental hypothesis
CONCLUSION
Findings
Future research
Full Text
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