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Science. 2015 May 1;348(6234):585-8. doi: 10.1126/science.1259114.

Retrotransposons. An RNA polymerase III subunit determines sites of retrotransposon integration.

Author information

1
Université Paris Diderot, Sorbonne Paris Cité, INSERM U944, CNRS UMR 7212, Institut Universitaire d'Hématologie, Hôpital St. Louis, 75010 Paris, France. Department CASER Conservatoire National des Arts et Métiers (Cnam), 75003 Paris, France.
2
Université Paris Diderot, Sorbonne Paris Cité, INSERM U944, CNRS UMR 7212, Institut Universitaire d'Hématologie, Hôpital St. Louis, 75010 Paris, France.
3
Department of Genetics, Cell Biology and Development and Center for Genome Engineering, University of Minnesota, Minneapolis, MN 55455, USA. Minnesota Supercomputing Institute, University of Minnesota, Minneapolis, MN 55455, USA.
4
IBiTec-S, Institut de Biologie Intégrative de la Cellule (I2BC), Commissariat à l'Energie Atomique et aux Energies Alternatives (CEA), CNRS, Université Paris-Sud, CP 22, CEA-Saclay, 91191 Gif-sur-Yvette, France.
5
Department of Genetics, Cell Biology and Development and Center for Genome Engineering, University of Minnesota, Minneapolis, MN 55455, USA.
6
Université Paris Diderot, Sorbonne Paris Cité, INSERM U944, CNRS UMR 7212, Institut Universitaire d'Hématologie, Hôpital St. Louis, 75010 Paris, France. pascale.lesage@inserm.fr.

Abstract

Mobile genetic elements are ubiquitous. Their integration site influences genome stability and gene expression. The Ty1 retrotransposon of the yeast Saccharomyces cerevisiae integrates upstream of RNA polymerase III (Pol III)-transcribed genes, yet the primary determinant of target specificity has remained elusive. Here we describe an interaction between Ty1 integrase and the AC40 subunit of Pol III and demonstrate that AC40 is the predominant determinant targeting Ty1 integration upstream of Pol III-transcribed genes. Lack of an integrase-AC40 interaction dramatically alters target site choice, leading to a redistribution of Ty1 insertions in the genome, mainly to chromosome ends. The mechanism of target specificity allows Ty1 to proliferate and yet minimizes genetic damage to its host.

PMID:
25931562
DOI:
10.1126/science.1259114
[Indexed for MEDLINE]
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