scholarly journals Genetic conflict, genomic imprinting and establishment of the epigenotype in relation to growth

Reproduction ◽  
2001 ◽  
pp. 185-193 ◽  
Author(s):  
T Moore
Keyword(s):  
Genomic Imprinting ◽  
Parental Investment ◽  
Tandem Repeats ◽  
Cpg Islands ◽  
Subsequent Development ◽  
Imprinted Genes ◽  
Growth Disorders ◽  
Genetic Loci ◽  
Mammalian Embryo ◽  
Genetic Conflict

Genomic imprinting is the process that differentially modifies the parental alleles at certain genetic loci in the parental germlines. Such modifications of DNA and chromatin are somatically heritable and cause unequal expression of the parental alleles during subsequent development. In mammals, imprinted genes encode a relatively small number of functionally heterogeneous proteins. Nevertheless, imprinted genes exert important effects, primarily on fetal development, and their deregulation is implicated in a variety of pathologies including sporadic, inherited and induced growth disorders. Imprinted loci show several unusual structural and functional characteristics that may be related to mechanistic aspects of mono-allelic expression or to modes of evolution of imprinted genetic loci. Typically, imprinted genes are clustered in certain genomic regions and have relatively reduced intronic DNA content relative to non-imprinted genes. In addition, their regulatory regions frequently contain a combination of features including tandem repeats associated with differentially methylated CpG islands and overlapping transcription of coding or non-coding RNAs. The evolution of imprinting can be understood as the stable outcome of sexual selection acting differently on the parental alleles of genes that influence parental investment in offspring. Consistent with this explanation, imprinted genes are expressed predominantly during embryonic and postnatal development in mammals and in the developing endosperm of plants, and maternal or paternal expression at imprinted loci is associated with reduced or increased parental investment, respectively. Such selective forces have implications for understanding mechanistic aspects of genome reprogramming in the early mammalian embryo.

scholarly journals A First-Stage Approximation to Identify New Imprinted Genes through Sequence Analysis of Its Coding Regions

2009 ◽  
Vol 2009 ◽  
pp. 1-7 ◽  
Author(s):  
Elias Daura-Oller ◽  
Maria Cabré ◽  
Miguel A. Montero ◽  
José L. Paternáin ◽  
Antoni Romeu
Keyword(s):  
Tandem Repeats ◽  
Cpg Islands ◽  
Imprinted Genes ◽  
Coding Region ◽  
Training Set ◽  
Principle Components Analysis ◽  
Coding Regions ◽  
Gene Coding ◽  
Components Analysis ◽  
Simple Repeats

In the present study, a positive training set of 30 known human imprinted gene coding regions are compared with a set of 72 randomly sampled human nonimprinted gene coding regions (negative training set) to identify genomic features common to human imprinted genes. The most important feature of the present work is its ability to use multivariate analysis to look at variation, at coding region DNA level, among imprinted and non-imprinted genes. There is a force affecting genomic parameters that appears through the use of the appropriate multivariate methods (principle components analysis (PCA) and quadratic discriminant analysis (QDA) to analyse quantitative genomic data. We show that variables, such as CG content, [bp]% CpG islands, [bp]% Large Tandem Repeats, and [bp]% Simple Repeats, are able to distinguish coding regions of human imprinted genes.

scholarly journals Genomic imprinting and the social brain

2006 ◽  
Vol 361 (1476) ◽  
pp. 2229-2237 ◽  
Author(s):  
Anthony R Isles ◽  
William Davies ◽  
Lawrence S Wilkinson
Keyword(s):  
Genomic Imprinting ◽  
Parental Investment ◽  
Social Groups ◽  
Monoallelic Expression ◽  
Imprinted Genes ◽  
Epigenetic Mark ◽  
Parental Allele ◽  
Intragenomic Conflict ◽  
Starting Point ◽  
The Social

Genomic imprinting refers to the parent-of-origin-specific epigenetic marking of a number of genes. This epigenetic mark leads to a bias in expression between maternally and paternally inherited imprinted genes, that in some cases results in monoallelic expression from one parental allele. Genomic imprinting is often thought to have evolved as a consequence of the intragenomic conflict between the parental alleles that occurs whenever there is an asymmetry of relatedness. The two main examples of asymmetry of relatedness are when there is partiality of parental investment in offspring (as is the case for placental mammals, where there is also the possibility of extended postnatal care by one parent), and in social groups where there is a sex-biased dispersal. From this evolutionary starting point, it is predicted that, at the behavioural level, imprinted genes will influence what can broadly be termed bonding and social behaviour. We examine the animal and human literature for examples of imprinted genes mediating these behaviours, and divide them into two general classes. Firstly, mother–offspring interactions (suckling, attachment and maternal behaviours) that are predicted to occur when partiality in parental investment in early postnatal offspring occurs; and secondly, adult social interactions, when there is an asymmetry of relatedness in social groups. Finally, we return to the evolutionary theory and examine whether there is a pattern of behavioural functions mediated by imprinted genes emerging from the limited data, and also whether any tangible predictions can be made with regards to the direction of action of genes of maternal or paternal origin.

scholarly journals Tandem repeats in the CpG islands of imprinted genes

Genomics ◽  
2006 ◽  
Vol 88 (3) ◽  
pp. 323-332 ◽  
Author(s):  
Barbara Hutter ◽  
Volkhard Helms ◽  
Martina Paulsen
Keyword(s):  
Tandem Repeats ◽  
Cpg Islands ◽  
Imprinted Genes

scholarly journals The Evolution of Genomic Imprinting

Genetics ◽  
1996 ◽  
Vol 144 (3) ◽  
pp. 1283-1295 ◽  
Author(s):  
Atsushi Mochizuki ◽  
Yasuhiko Takeda ◽  
Yoh Iwasa
Keyword(s):  
Growth Factor ◽  
Genomic Imprinting ◽  
Parental Origin ◽  
Coding Region ◽  
Placental Development ◽  
Genetic Conflict ◽  
Multiple Partners ◽  
Zygotic Gene ◽  
Mammalian Genes ◽  
Maternal Resources

Abstract In some mammalian genes, the paternally and maternally derived alleles are expressed differently: this phenomenon is called genomic imprinting. Here we study the evolution of imprinting using multivariate quantitative genetic models to examine the feasibility of the genetic conflict hypothesis. This hypothesis explains the observed imprinting patterns as an evolutionary outcome of the conflict between the paternal and maternal alleles. We consider the expression of a zygotic gene, which codes for an embryonic growth factor affecting the amount of maternal resources obtained through the placenta. We assume that the gene produces the growth factor in two different amounts depending on its parental origin. We show that genomic imprinting evolves easily if females have some probability of multiple partners. This is in conflict with the observation that not all genes controlling placental development are imprinted and that imprinting in some genes is not conserved between mice and humans. We show however that deleterious mutations in the coding region of the gene create selection against imprinting.

scholarly journals Genomic imprinting in germ cells: imprints are under control

Reproduction ◽  
2010 ◽  
Vol 140 (3) ◽  
pp. 411-423 ◽  
Author(s):  
Philippe Arnaud
Keyword(s):  
Dna Methylation ◽  
Genomic Imprinting ◽  
Germ Cells ◽  
Imprinted Genes ◽  
Regulatory Sequences ◽  
Sequence Specificity ◽  
Maternal Allele ◽  
Primary Sequence ◽  
Chromatin Configuration

The cis-acting regulatory sequences of imprinted gene loci, called imprinting control regions (ICRs), acquire specific imprint marks in germ cells, including DNA methylation. These epigenetic imprints ensure that imprinted genes are expressed exclusively from either the paternal or the maternal allele in offspring. The last few years have witnessed a rapid increase in studies on how and when ICRs become marked by and subsequently maintain such epigenetic modifications. These novel findings are summarised in this review, which focuses on the germline acquisition of DNA methylation imprints and particularly on the combined role of primary sequence specificity, chromatin configuration, non-histone proteins and transcriptional events.

scholarly journals Genomic Imprinting of Dopa decarboxylase in Heart and Reciprocal Allelic Expression with Neighboring Grb10

2007 ◽  
Vol 28 (1) ◽  
pp. 386-396 ◽  
Author(s):  
Trevelyan R. Menheniott ◽  
Kathryn Woodfine ◽  
Reiner Schulz ◽  
Andrew J. Wood ◽  
David Monk ◽  
...  
Keyword(s):  
Genomic Imprinting ◽  
Promoter Region ◽  
Germ Line ◽  
Differential Methylation ◽  
Dopa Decarboxylase ◽  
Imprinted Genes ◽  
Chromosome 11 ◽  
Imprinted Gene ◽  
Line Methylation ◽  
Intron 1

ABSTRACT By combining a tissue-specific microarray screen with mouse uniparental duplications, we have identified a novel imprinted gene, Dopa decarboxylase (Ddc), on chromosome 11. Ddc_exon1a is a 2-kb transcript variant that initiates from an alternative first exon in intron 1 of the canonical Ddc transcript and is paternally expressed in trabecular cardiomyocytes of the embryonic and neonatal heart. Ddc displays tight conserved linkage with the maternally expressed and methylated Grb10 gene, suggesting that these reciprocally imprinted genes may be coordinately regulated. In Dnmt3L mutant embryos that lack maternal germ line methylation imprints, we show that Ddc is overexpressed and Grb10 is silenced. Their imprinting is therefore dependent on maternal germ line methylation, but the mechanism at Ddc does not appear to involve differential methylation of the Ddc_exon1a promoter region and may instead be provided by the oocyte mark at Grb10. Our analysis of Ddc redefines the imprinted Grb10 domain on mouse proximal chromosome 11 and identifies Ddc_exon1a as the first example of a heart-specific imprinted gene.

scholarly journals Transposons and Tandem Repeats Are Not Involved in the Control of Genomic Imprinting at the MEDEA Locus in Arabidopsis

2004 ◽  
Vol 69 (0) ◽  
pp. 465-476 ◽  
Author(s):  
C. SPILLANE ◽  
C. BAROUX ◽  
J.-M. ESCOBAR-RESTREPO ◽  
D.R. PAGE ◽  
S. LAOUEILLE ◽  
...  
Keyword(s):  
Genomic Imprinting ◽  
Tandem Repeats

scholarly journals Transposons, Tandem Repeats, and the Silencing of Imprinted Genes

2004 ◽  
Vol 69 (0) ◽  
pp. 371-380 ◽  
Author(s):  
R. MARTIENSSEN ◽  
Z. LIPPMAN ◽  
B. MAY ◽  
M. RONEMUS ◽  
M. VAUGHN
Keyword(s):  
Tandem Repeats ◽  
Imprinted Genes

scholarly journals Genomic imprinting and its role in ethiology of human hereditary diseases

2004 ◽  
Vol 3 (3) ◽  
pp. 8-17
Author(s):  
S. A. Nazarenko
Keyword(s):  
Gene Expression ◽  
Genomic Imprinting ◽  
Special Class ◽  
Growth And Development ◽  
Epigenetic Inheritance ◽  
Hereditary Diseases ◽  
Parental Origin ◽  
Imprinted Genes ◽  
Methylation Of Dna ◽  
Differential Gene

Genomic imprinting is a form of non-Mendelian epigenetic inheritance that is defined by differential gene expression depending on its parental origin — maternal or paternal. It is known about 60 imprinted genes many of which effect significantly on the fetus growth and development. Methylation of DNA cytosine bases that defines the interaction of DNA and proteins identifying the modified bases and controls the gene expression through chromatin compacting-decompacting mechanism, is a main epigenetic genom modifier. Disturbances in monoallelic gene expression lead to the development of a special class of human hereditary diseases — genomic imprinting diseases.

Contribution of Placental Genomic Imprinting and Identification of Imprinted Genes

2014 ◽  
pp. 275-284 ◽  
Author(s):  
Laura C. Kusinski ◽  
Wendy N. Cooper ◽  
Ionel Sandovici ◽  
Miguel Constância
Keyword(s):  
Genomic Imprinting ◽  
Imprinted Genes
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