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 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 Tandem Repeat Hypothesis in Imprinting: Deletion of a Conserved Direct Repeat Element Upstream of H19 Has No Effect on Imprinting in the Igf2-H19 Region

2004 ◽  
Vol 24 (13) ◽  
pp. 5650-5656 ◽  
Author(s):  
Annabelle Lewis ◽  
Kohzoh Mitsuya ◽  
Miguel Constancia ◽  
Wolf Reik
Keyword(s):  
Tandem Repeat ◽  
Tandem Repeats ◽  
Direct Repeat ◽  
Regulatory Elements ◽  
Repeat Element ◽  
Allelic Expression ◽  
Differentially Methylated Region ◽  
Paternal Allele ◽  
Imprinted Genes ◽  
Allele Specific

ABSTRACT Igf2 and H19 are reciprocally imprinted genes on mouse distal chromosome 7. They share several regulatory elements, including a differentially methylated region (DMR) upstream of H19 that is paternally methylated throughout development. The cis-acting sequence requirements for targeting DNA methylation to the DMR remain unknown; however, it has been suggested that direct tandem repeats near DMRs could be involved. Previous studies of the imprinted Rasgrf1 locus demonstrate indeed that a direct repeat element adjacent to a DMR is responsible for establishing paternal allele-specific methylation at the DMR and therefore allelic expression of the Rasgrf1 transcript. We identified a prominent and conserved direct tandem repeat 1 kb upstream of the H19 DMR and proposed that it played a similar role in imprinted regulation of H19. To test our hypothesis, we generated mice harboring a 1.7-kb targeted deletion of the direct repeat element and analyzed fetal growth, allelic expression, and methylation within the Igf2-H19 region. Surprisingly the deletion had no effect on imprinting. These results together with deletions of other repeats close to imprinted genes suggest that direct repeats may not be important for the targeting of methylation at the majority of imprinted loci and that the Rasgrf1 locus may be an exception to this rule.

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 Specific Differentially Methylated Domain Sequences Direct the Maintenance of Methylation at Imprinted Genes

2006 ◽  
Vol 26 (22) ◽  
pp. 8347-8356 ◽  
Author(s):  
Bonnie Reinhart ◽  
Ariane Paoloni-Giacobino ◽  
J. Richard Chaillet
Keyword(s):  
Tandem Repeats ◽  
Germ Line ◽  
Gene Clusters ◽  
Imprinted Genes ◽  
Specific Expression ◽  
Cpg Dinucleotides ◽  
Parental Allele ◽  
Epigenetic State ◽  
Genomic Reprogramming ◽  
Genomic Signal

ABSTRACT Landmark features of imprinted genes are differentially methylated domains (DMDs), in which one parental allele is methylated on CpG dinucleotides and the opposite allele is unmethylated. Genetic experiments in the mouse have shown that DMDs are required for the parent-specific expression of linked clusters of imprinted genes. To understand the mechanism whereby the differential methylation is established and maintained, we analyzed a series of transgenes containing DMD sequences and showed that imperfect tandem repeats from DMDs associated with the Snurf/Snrpn, Kcnq1, and Igf2r gene clusters govern transgene imprinting. For the Igf2r DMD the minimal imprinting signal is two unit copies of the tandem repeat. This imprinted transgene behaves identically to endogenous imprinted genes in Dnmt1o and Dnmt3L mutant mouse backgrounds. The primary function of the imprinting signal within the transgene DMD is to maintain, during embryogenesis and a critical period of genomic reprogramming, parent-specific DNA methylation states established in the germ line. This work advances our understanding of the imprinting mechanism by defining a genomic signal that dependably perpetuates an epigenetic state during postzygotic development.

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

Quantitative evaluation of post-bone marrow transplant engraftment status using fluorescent-labeled variable number of tandem repeats

2000 ◽  
Vol 05 (2) ◽  
pp. 129-138
Author(s):  
Robert A. Luhm ◽  
Daniel B. Bellissimo ◽  
Arejas J. Uzgiris ◽  
William R. Drobyski ◽  
Martin J. Hessner
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplant ◽  
Quantitative Evaluation ◽  
Tandem Repeats ◽  
Marrow Transplant ◽  
Variable Number

Diversity of Primary Structures of the Carboxy-terminal Regions of Mammalian Fibrinogen Aα-Chains

1993 ◽  
Vol 69 (04) ◽  
pp. 351-360 ◽  
Author(s):  
Masahiro Murakawa ◽  
Takashi Okamura ◽  
Takumi Kamura ◽  
Tsunefumi Shibuya ◽  
Mine Harada ◽  
...  
Keyword(s):  
Amino Acid ◽  
Rhesus Monkey ◽  
Syrian Hamster ◽  
Tandem Repeats ◽  
Mammalian Species ◽  
Amino Acid Sequences ◽  
Point Of View ◽  
Cross Linking ◽  
Amino Terminal ◽  
Rgd Sequence

SummaryThe partial amino acid sequences of fibrinogen Aα-chains from five mammalian species have been inferred by means of the polymerase chain reaction (PCR). From the genomic DNA of the rhesus monkey, pig, dog, mouse and Syrian hamster, the DNA fragments coding for α-C domains in the Aα-chains were amplified and sequenced. In all species examined, four cysteine residues were always conserved at the homologous positions. The carboxy- and amino-terminal portions of the α-C domains showed a considerable homology among the species. However, the sizes of the middle portions, which corresponded to the internal repeat structures, showed an apparent variability because of several insertions and/or deletions. In the rhesus monkey, pig, mouse and Syrian hamster, 13 amino acid tandem repeats fundamentally similar to those in humans and the rat were identified. In the dog, however, tandem repeats were found to consist of 18 amino acids, suggesting an independent multiplication of the canine repeats. The sites of the α-chain cross-linking acceptor and α2-plasmin inhibitor cross-linking donor were not always evolutionally conserved. The arginyl-glycyl-aspartic acid (RGD) sequence was not found in the amplified region of either the rhesus monkey or the pig. In the canine α-C domain, two RGD sequences were identified at the homologous positions to both rat and human RGD S. In the Syrian hamster, a single RGD sequence was found at the same position to that of the rat. Triplication of the RGD sequences was seen in the murine fibrinogen α-C domain around the homologous site to the rat RGDS sequence. These findings are of some interest from the point of view of structure-function and evolutionary relationships in the mammalian fibrinogen Aα-chains.

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