Construction and evolution of imprinted loci in mammals

被引:73
作者
Hore, Timothy A. [1 ]
Rapkins, Robert W. [1 ]
Graves, Jennifer A. Marshall [1 ]
机构
[1] Australian Natl Univ, Res Sch Biol Sci, Canberra, ACT 2601, Australia
关键词
D O I
10.1016/j.tig.2007.07.003
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Genomic imprinting first evolved in mammals around the time that humans last shared a common ancestor with marsupials and monotremes (180-210 million years ago). Recent comparisons of large imprinted domains in these divergent mammalian groups have shown that imprinting evolved haphazardly at various times in different lineages, perhaps driven by different selective forces. Surprisingly, some imprinted domains were formed relatively recently, using non-imprinted components acquired from unexpected genomic regions. Rearrangement and the insertion of retrogenes, small nucleolar RNAs, microRNAs, differential CpG methylation and control by non-coding RNA often accompanied the acquisition of imprinting. Here, we use comparisons between different mammalian groups to chart the course of evolution of two related epigenetic regulatory systems in mammals: genomic imprinting and X-chromosome inactivation.
引用
收藏
页码:440 / 448
页数:9
相关论文
共 88 条
[1]   Regulation of placental efficiency for nutrient transport by imprinted genes [J].
Angiolini, E ;
Fowden, A ;
Coan, P ;
Sandovici, I ;
Smith, P ;
Dean, W ;
Burton, G ;
Tycko, B ;
Reik, W ;
Sibley, C ;
Constância, M .
PLACENTA, 2006, 27 :S98-S102
[2]   A GENE FROM THE REGION OF THE HUMAN X-INACTIVATION CENTER IS EXPRESSED EXCLUSIVELY FROM THE INACTIVE X-CHROMOSOME [J].
BROWN, CJ ;
BALLABIO, A ;
RUPERT, JL ;
LAFRENIERE, RG ;
GROMPE, M ;
TONLORENZI, R ;
WILLARD, HF .
NATURE, 1991, 349 (6304) :38-44
[3]   Just how happy is the happy puppet? An emotion signaling and kinship theory perspective, on the behavioral phenotype of children with Angelman Syndrome [J].
Brown, WM ;
Consedine, NS .
MEDICAL HYPOTHESES, 2004, 63 (03) :377-385
[4]   A candidate model for Angelman syndrome in the mouse [J].
Cattanach, BM ;
Barr, JA ;
Beechey, CV ;
Martin, J ;
Noebels, J ;
Jones, J .
MAMMALIAN GENOME, 1997, 8 (07) :472-478
[5]   Retrotransposed genes such as Frat3 in the mouse Chromosome 7C Prader-Willi syndrome region acquire the imprinted status of their insertion site [J].
Chai, JH ;
Locke, DP ;
Ohta, T ;
Greally, JM ;
Nicholls, RD .
MAMMALIAN GENOME, 2001, 12 (11) :813-821
[6]   The Prader-Willi syndrome imprinting center activates the paternally expressed murine Ube3a antisense transcript but represses paternal Ube3a [J].
Chamberlain, SJ ;
Brannan, CI .
GENOMICS, 2001, 73 (03) :316-322
[7]   Human-ovine comparative sequencing of a 250-kb imprinted domain encompassing the callipyge (clpg) locus and identification of six imprinted transcripts:: DLK1, DAT, GTL2, PEG11, antiPEG11, and MEG8 [J].
Charlier, C ;
Segers, K ;
Wagenaar, D ;
Karim, L ;
Berghams, S ;
Jaillon, O ;
Shay, T ;
Weissenbach, J ;
Cockett, N ;
Gyapay, G ;
Georges, M .
GENOME RESEARCH, 2001, 11 (05) :850-862
[8]   Comparative sequence analysis of the X-inactivation center region in mouse, human, and bovine [J].
Chureau, C ;
Prissette, M ;
Bourdet, A ;
Barbe, V ;
Cattolico, L ;
Jones, L ;
Eggen, A ;
Avner, P ;
Duret, L .
GENOME RESEARCH, 2002, 12 (06) :894-908
[9]   Polar overdominance at the Ovine callipyge locus [J].
Cockett, NE ;
Jackson, SP ;
Shay, TL ;
Farnir, F ;
Berghmans, S ;
Snowder, GD ;
Nielsen, DM ;
Georges, M .
SCIENCE, 1996, 273 (5272) :236-238
[10]  
Cooper D.W., 1993, Seminars in Developmental Biology, V4, P117, DOI 10.1006/sedb.1993.1014