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Published online before print February 6, 2008, 10.1101/gr.7146408
Genome Res. 18:359-369, 2008
©2008 by Cold Spring Harbor Laboratory Press; ISSN 1088-9051/08 $5.00
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Letter

Chromodomains direct integration of retrotransposons to heterochromatin

Xiang Gao1,3, Yi Hou1, Hirotaka Ebina2, Henry L. Levin2, and Daniel F. Voytas1,4

1 Department of Genetics, Development & Cell Biology, Iowa State University, Ames, Iowa 50011, USA; 2 Section on Eukaryotic Transposable Elements, Laboratory of Gene Regulation and Development, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA

The enrichment of mobile genetic elements in heterochromatin may be due, in part, to targeted integration. The chromoviruses are Ty3/gypsy retrotransposons with chromodomains at their integrase C termini. Chromodomains are logical determinants for targeting to heterochromatin, because the chromodomain of heterochromatin protein 1 (HP1) typically recognizes histone H3 K9 methylation, an epigenetic mark characteristic of heterochromatin. We describe three groups of chromoviruses based on amino acid sequence relationships of their integrase C termini. Genome sequence analysis indicates that representative chromoviruses from each group are enriched in gene-poor regions of the genome relative to other retrotransposons, and when fused to fluorescent marker proteins, the chromodomains target proteins to specific subnuclear foci coincident with heterochromatin. The chromodomain of the fungal element, MAGGY, interacts with histone H3 dimethyl- and trimethyl-K9, and when the MAGGY chromodomain is fused to integrase of the Schizosaccharomyces pombe Tf1 retrotransposon, new Tf1 insertions are directed to sites of H3 K9 methylation. Repetitive sequences such as transposable elements trigger the RNAi pathway resulting in their epigenetic modification. Our results suggest a dynamic interplay between retrotransposons and heterochromatin, wherein mobile elements recognize heterochromatin at the time of integration and then perpetuate the heterochromatic mark by triggering epigenetic modification.

3 Present address: Department of Biology, 1001 East Third Street, Indiana University, Bloomington, Indiana 47405, USA.

4 Corresponding author.

E-mail Voytas{at}iastate.edu; fax (515) 294-7155.

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

Article published online before print. Article and publication date are at http://www.genome.org/cgi/doi/10.1101/gr.7146408


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