| View Larger Image | Genetic network interactions among replication, repair and nuclear pore deficiencies in yeast [An article from: DNA Repair] | Digitalby S. Loeillet (Author), B. Palancade (Author), M. Cartron (Author), A. Thierry (Author)
| List Price: | $10.95 | | | Available: | Available for download now |
| | Binding: | Digital | | Publisher: | Elsevier | | Publication Date: | April 04, 2005 |
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Product Description
This digital document is a journal article from DNA Repair, published by Elsevier in 2005. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.Description: The yeast RAD27 gene encodes a functional homolog of the mammalian FEN1 protein, a structure-specific endo/exonuclease which plays an important role in DNA replication and repair. Previous genetic interaction studies, including a synthetic genetic array (SGA) analysis, showed that the survival of rad27@D cells requires several DNA metabolic processes, in particular those mediated by all members of the Rad52-dependent recombinational repair pathway. Here, we report the results of our SGA analysis of the collection of non-essential yeast genes against the rad27@D mutation, which resulted in the identification of a novel synthetic lethal interaction conferred by mutations affecting the Nup84 nuclear pore subcomplex (nup133@D, nup120@Dand nup84@D). Additional screens showed that all Rad52 group genes are required for the survival of the nup133@D and nup120@D mutants, which are defective in nuclear pore distribution and mRNA export, but not of the nup133@DN mutant, which is solely defective in pore distribution. This requirement for the DNA double-strand break (DSB) repair pathway is consistent with the observation that, like rad27@D, the nup133@D, nup120@D and nup84@D mutants are sensitive to methyl methanesulfonate (MMS). Furthermore, nup133@D cells exhibit an increased number of spontaneous DNA repair foci containing Rad52. Altogether, these data suggest that the pathological interactions between the rad27@D and specific nup@D mutations result from the accumulation of unrepaired DNA damages. |
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