Retrotransposon reverse-transcriptase-mediated repair of chromosomal breaks

• Published in: Nature (London) Vol. 383; no. 6601; pp. 641 - 644
• Main Authors: Teng, Shu-Chun, Kim, Bohye, Gabriel, Abram
• Format: Journal Article
• Language: English
• Published: London Nature Publishing 17.10.1996; Nature Publishing Group
• Subjects: Animals; Biochemistry; Biological and medical sciences; Chromosome Breakage; Crithidia - genetics; Deoxyribonucleic acid; DNA; DNA - metabolism; DNA Repair; Fundamental and applied biological sciences. Psychology; Genes; Histidine - metabolism; Humans; Molecular and cellular biology; Molecular genetics; Molecular Sequence Data; Mutagenesis. Repair; Recombinant Proteins - metabolism; Retroelements; RNA-Directed DNA Polymerase - metabolism; Saccharomyces cerevisiae; Saccharomyces cerevisiae - genetics; Yeast; Yeasts; Retrotransposon; Yeast; RNA-directed DNA polymerase; Enzyme; Transferases; Model study; Transposable element; Fungi; Double strand break; Nucleotidyltransferases; Chromosome break; Nonhomologous recombination; Ascomycetes; Repair; Saccharomyces cerevisiae; Thallophyta
• ISSN: 0028-0836; 1476-4687
• DOI: 10.1038/383641a0

The abundance of short and long interspersed nuclear sequences (SINEs and LINEs) and pseudogenes in eukaryotic genomes indicates that reverse transcriptase (RT)-mediated phenomena are important in genome evolution. However, the mechanisms involved in their spread are largely unknown. We have developed a selection system in the yeast Saccharomyces cerevisiae to test whether RT-mediated events could be linked to the repair of double-strand breaks (DSBs). Here we show that DSBs can be fixed by the insertion of complementary DNAs at the break site. In the presence of functional RT (from human L1, yeast Tyl or Crithidia CRE1), and in the absence of homologous recombination, an HO endonuclease-induced DSB at the mating type (MAT) locus is the primary site at which a marked cDNA is observed among surviving cells. The structure and junctional sequences of these insertions suggest that repair occurs primarily by non-homologous recombination. Our data support a role for endogenous retroelements in the repair of chromosomal breaks.