This Article Full Text Full Text (PDF) Supplemental Research Data The Chicken Genome All Versions of this Article: gr.2689805v1 15/1/146    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Paulsen, M. Articles by Walter, J. Search for Related Content PubMed PubMed Citation Articles by Paulsen, M. Articles by Walter, J. Social Bookmarking                   What's this?

Chicken Special/Letter

Evolution of the Beckwith-Wiedemann syndrome region in vertebrates

Universität des Saarlandes, FR 8.3 Biowissenschaften, Genetik/Epigenetik, Postfach 151150, D-66041 Saarbrücken, Germany

In the animal kingdom, genomic imprinting appears to be restricted to mammals. It remains an open question how structural features for imprinting evolved in mammalian genomes. The clustering of genes around imprinting control centers (ICs) is regarded as a hallmark for the coordinated imprinted regulation. Hence imprinted clusters might be structurally distinct between mammals and nonimprinted vertebrates. To address this question we compared the organization of the Beckwith Wiedemann syndrome (BWS) gene cluster in mammals, chicken, Fugu (pufferfish), and zebrafish. Our analysis shows that gene synteny is apparently well conserved between mammals and birds, and is detectable but less pronounced in fish. Hence, clustering apparently evolved during vertebrate radiation and involved two major duplication events that took place before the separation of the fish and mammalian lineages. A cross-species analysis of imprinting center regions showed that some structural features can already be recognized in nonimprinted amniotes in one of the imprinting centers (IC2). In contrast, the imprinting center IC1 is absent in chicken. This suggests a progressive and stepwise evolution of imprinting control elements. In line with that, imprinting centers in mammals apparently exhibit a high degree of structural and sequence variation despite conserved epigenetic marking.

¹ Corresponding author.
E-mail m.paulsen{at}mx.uni-saarland.de; fax 49 681-302 2703.

[Supplemental material is available online at www.genome.org.]

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				F. Mohammad, R. R. Pandey, T. Nagano, L. Chakalova, T. Mondal, P. Fraser, and C. Kanduri Kcnq1ot1/Lit1 Noncoding RNA Mediates Transcriptional Silencing by Targeting to the Perinucleolar Region Mol. Cell. Biol., June 1, 2008; 28(11): 3713 - 3728. [Abstract] [Full Text] [PDF]

				P. B. Siegel, J. B. Dodgson, and L. Andersson Progress from Chicken Genetics to the Chicken Genome Poult. Sci., December 1, 2006; 85(12): 2050 - 2060. [Abstract] [Full Text] [PDF]

				D. Mancini-DiNardo, S. J.S. Steele, J. M. Levorse, R. S. Ingram, and S. M. Tilghman Elongation of the Kcnq1ot1 transcript is required for genomic imprinting of neighboring genes. Genes & Dev., May 15, 2006; 20(10): 1268 - 1282. [Abstract] [Full Text] [PDF]