Journal
GENETICS
Volume 181, Issue 1, Pages 301-311Publisher
GENETICS SOCIETY AMERICA
DOI: 10.1534/genetics.108.096636
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Funding
- National Institutes of Health [CIA 1651.9]
- Carnegie Institution of Washington
- NATIONAL CANCER INSTITUTE [P01CA016519] Funding Source: NIH RePORTER
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Over one-third of human genome sequence is a product of non-LTR retrotransposition. The retrotransposon that currently drives this process in humans is the highly abundant. LINE-1 (L1) element. Despite the ubiquitous nature of L1's in mammals, we still lack a complete mechanistic understanding of the L1 replication cycle and how it is regulated. To generate a genetically amenable model for non-LTR retrotransposition, we have reengineered the Zorro3 retrotransposon, an L1 homolog from Candida albicans, for use in the budding yeast Saccharomyces cerevisiae. We found that S. cerevisiae, which has no endogenons L1 homologs or remnants, can still support Zorro3 retrotransposition. Analysis of Zorro3 mutants and insertion structures suggest that this is authentic L1-like retrotransposition with remarkable resemblance to mammalian L1-mediated events. This suggests that S. cerevisiae has unexpectedly retained the basal host. machinery required for L1 retrotransposition. This model will also serve as a powerful system to study the cell biology of L1 elements and for the genetic identification and characterization of cellular factors involved in L1 retrotransposition.
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