Skip NavigationSkip to Content
Return Return to Search Results

The Saccharomyces cerevisiae DNA recombination and repair functions of the RAD52 epistasis group inhibit Tyl transposition

  1. Author:
    Rattray, A. J.
    Shafer, B. K.
    Garfinkel, D. J.

  2. Author Address

    Rattray AJ NCI, Gene Regulat & Chromosome Biol Lab, ABL Basic Res Program, FCRDC POB B,Bldg 539,Rm 151 Frederick, MD 21702 USA NCI, Gene Regulat & Chromosome Biol Lab, ABL Basic Res Program, FCRDC Frederick, MD 21702 USA
    1. Year: 2000
  2. Journal: Genetics
    1. 154
    2. 2
    3. Pages: 543-556
  4. Type of Article: Review
  1. Abstract:

    RNA transcribed from the Saccharomyces cerevisiae retrotransposon Ty1 accumulates to a high level in mitotically growing haploid cells, yet transposition occurs at very low frequencies. The product of reverse transcription is a linear double-stranded DNA molecule that reenters the genome by either Ty1-integrase-mediated insertion or homologous recombination with one of the preexisting genomic Ty1 (or delta) elements. Here we examine the role of the cellular homologous recombination functions on Ty1 transposition. We find that transposition is elevated in cells mutated for genes in the RAD52 recombinational repair pathway, such as RAD50, RAD51, RAD52 RAD54, or RAD57, or in the DNA ligase I gene CDC9, but is not elevated in cells mutated in the DNA repair functions encoded by the RAD1, RAD2, or MSH2 genes. The increase in Ty1 transposition observed when genes in the RAD52 recombinational pathway are mutated is not associated with a significant increase in Ty1 RNA or proteins. However, unincorporated Ty1 cDNA levels are markedly elevated. These results suggest that members of the RAD52 recombinational repair pathway inhibit Ty1 post-translationally by influencing the fate of Ty1 cDNA. [References: 135]

    See More

  1. Keywords:

External Sources

  1. No sources found.

Library Notes

  1. No notes added.
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel